49 results on '"Caro, Marta"'
Search Results
2. Cortistatin as a Novel Multimodal Therapy for the Treatment of Parkinson’s Disease
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Junta de Andalucía, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia e Innovación (España), Conselho Nacional de Desenvolvimento Científico e Tecnológico (Brasil), Serrano-Martínez, Ignacio, Pedreño, M., Castillo-González, Julia, Ferraz-de-Paula, Viviane, Vargas Rodríguez, Pablo, Forte-Lago, Irene, Caro, Marta, Campos-Salinas, Jenny, Villadiego, Javier, Peñalver, Pablo, Morales, Juan Carlos, Delgado, Mario, González-Rey, Elena, Junta de Andalucía, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Ministerio de Ciencia e Innovación (España), Conselho Nacional de Desenvolvimento Científico e Tecnológico (Brasil), Serrano-Martínez, Ignacio, Pedreño, M., Castillo-González, Julia, Ferraz-de-Paula, Viviane, Vargas Rodríguez, Pablo, Forte-Lago, Irene, Caro, Marta, Campos-Salinas, Jenny, Villadiego, Javier, Peñalver, Pablo, Morales, Juan Carlos, Delgado, Mario, and González-Rey, Elena
- Abstract
Parkinson’s disease (PD) is a complex disorder characterized by the impairment of the dopaminergic nigrostriatal system. PD has duplicated its global burden in the last few years, becoming the leading neurological disability worldwide. Therefore, there is an urgent need to develop innovative approaches that target multifactorial underlying causes to potentially prevent or limit disease progression. Accumulating evidence suggests that neuroinflammatory responses may play a pivotal role in the neurodegenerative processes that occur during the development of PD. Cortistatin is a neuropeptide that has shown potent anti-inflammatory and immunoregulatory effects in preclinical models of autoimmune and neuroinflammatory disorders. The goal of this study was to explore the therapeutic potential of cortistatin in a well-established preclinical mouse model of PD induced by acute exposure to the neurotoxin 1-methil-4-phenyl1-1,2,3,6-tetrahydropyridine (MPTP). We observed that treatment with cortistatin mitigated the MPTP-induced loss of dopaminergic neurons in the substantia nigra and their connections to the striatum. Consequently, cortistatin administration improved the locomotor activity of animals intoxicated with MPTP. In addition, cortistatin diminished the presence and activation of glial cells in the affected brain regions of MPTP-treated mice, reduced the production of immune mediators, and promoted the expression of neurotrophic factors in the striatum. In an in vitro model of PD, treatment with cortistatin also demonstrated a reduction in the cell death of dopaminergic neurons that were exposed to the neurotoxin. Taken together, these findings suggest that cortistatin could emerge as a promising new therapeutic agent that combines anti-inflammatory and neuroprotective properties to regulate the progression of PD at multiple levels.
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- 2024
3. Cortistatin as a Novel Multimodal Therapy for the Treatment of Parkinson’s Disease
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Serrano-Martínez, Ignacio, primary, Pedreño, Marta, additional, Castillo-González, Julia, additional, Ferraz-de-Paula, Viviane, additional, Vargas-Rodríguez, Pablo, additional, Forte-Lago, Irene, additional, Caro, Marta, additional, Campos-Salinas, Jenny, additional, Villadiego, Javier, additional, Peñalver, Pablo, additional, Morales, Juan Carlos, additional, Delgado, Mario, additional, and González-Rey, Elena, additional
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- 2024
- Full Text
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4. Alkylated resveratrol prodrugs and metabolites as potential therapeutics for neurodegenerative diseases
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Peñalver, Pablo, Belmonte-Reche, Efres, Adán, Norma, Caro, Marta, Mateos-Martín, María Luisa, Delgado, Mario, González-Rey, Elena, and Morales, Juan Carlos
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- 2018
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5. Cortistatin deficiency reveals a dysfunctional brain endothelium with impaired gene pathways, exacerbated immune activation, and disrupted barrier integrity
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Ministerio de Economía y Competitividad (España), Ministerio de Ciencia e Innovación (España), Ministerio de Universidades (España), Castillo-González, J., Ruiz, J.L., Serrano-Martínez, Ignacio, Forte-Lago, Irene, Ubago-Rodriguez, Ana, Caro, Marta, Pérez-Gómez, J. M., Benítez-Troncoso, Alejandro, Andrés-León, Eduardo, Sánchez-Navarro, Macarena, Luque, Raúl M., González-Rey, Elena, Ministerio de Economía y Competitividad (España), Ministerio de Ciencia e Innovación (España), Ministerio de Universidades (España), Castillo-González, J., Ruiz, J.L., Serrano-Martínez, Ignacio, Forte-Lago, Irene, Ubago-Rodriguez, Ana, Caro, Marta, Pérez-Gómez, J. M., Benítez-Troncoso, Alejandro, Andrés-León, Eduardo, Sánchez-Navarro, Macarena, Luque, Raúl M., and González-Rey, Elena
- Abstract
Background: Brain activity governing cognition and behaviour depends on the fine-tuned microenvironment provided by a tightly controlled blood–brain barrier (BBB). Brain endothelium dysfunction is a hallmark of BBB breakdown in most neurodegenerative/neuroinflammatory disorders. Therefore, the identification of new endogenous molecules involved in endothelial cell disruption is essential to better understand BBB dynamics. Cortistatin is a neuroimmune mediator with anti-inflammatory and neuroprotective properties that exerts beneficial effects on the peripheral endothelium. However, its role in the healthy and injured brain endothelium remains to be evaluated. Herein, this study aimed to investigate the potential function of endogenous and therapeutic cortistatin in regulating brain endothelium dysfunction in a neuroinflammatory/neurodegenerative environment. Methods: Wild-type and cortistatin-deficient murine brain endothelium and human cells were used for an in vitro barrier model, where a simulated ischemia-like environment was mimicked. Endothelial permeability, junction integrity, and immune response in the presence and absence of cortistatin were evaluated using different size tracers, immunofluorescence labelling, qPCR, and ELISA. Cortistatin molecular mechanisms underlying brain endothelium dynamics were assessed by RNA-sequencing analysis. Cortistatin role in BBB leakage was evaluated in adult mice injected with LPS. Results: The endogenous lack of cortistatin predisposes endothelium weakening with increased permeability, tight-junctions breakdown, and dysregulated immune activity. We demonstrated that both damaged and uninjured brain endothelial cells isolated from cortistatin-deficient mice, present a dysregulated and/or deactivated genetic programming. These pathways, related to basic physiology but also crucial for the repair after damage (e.g., extracellular matrix remodelling, angiogenesis, response to oxygen, signalling, and metabolites transport), ar
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- 2023
6. Correction to: The atypical RhoGTPase RhoE/Rnd3 is a key molecule to acquire a neuroprotective phenotype in microglia
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Neubrand, Veronika E., Forte-Lago, Irene, Caro, Marta, and Delgado, Mario
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- 2019
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7. The atypical RhoGTPase RhoE/Rnd3 is a key molecule to acquire a neuroprotective phenotype in microglia
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Neubrand, Veronika E., Forte-Lago, Irene, Caro, Marta, and Delgado, Mario
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- 2018
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8. Adrenomedullin protects from experimental autoimmune encephalomyelitis at multiple levels
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Pedreño, Marta, Morell, Maria, Robledo, Gema, Souza-Moreira, Luciana, Forte-Lago, Irene, Caro, Marta, O’Valle, Francisco, Ganea, Doina, and Gonzalez-Rey, Elena
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- 2014
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9. Cortistatin regulates fibrosis and myofibroblast activation in experimental hepatotoxic¿and cholestatic¿induced liver injury.
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Ministerio de Ciencia e Innovación (España), Junta de Andalucía, Benitez, Raquel, Caro, Marta, Andrés-León, Eduardo, O'Valle, Francisco, Delgado, Mario, Ministerio de Ciencia e Innovación (España), Junta de Andalucía, Benitez, Raquel, Caro, Marta, Andrés-León, Eduardo, O'Valle, Francisco, and Delgado, Mario
- Abstract
Background and Purpose Liver fibrosis induced by chronic hepatic injury remains a major cause of morbidity and mortality worldwide. Identification of susceptibility/prognosis factors and new therapeutic tools for treating hepatic fibrotic disorders are urgent medical needs. Cortistatin is a neuropeptide with potent anti-inflammatory and anti-fibrotic activities in lung that binds to receptors that are expressed in liver fibroblasts and hepatic stellate cells. We evaluated the capacity of cortistatin to regulate liver fibrosis. Experimental Approach We experimentally induced liver fibrosis in mice by chronic CCl4 exposure and bile duct ligation and evaluated the histopathological signs and fibrotic markers. Key Results Hepatic expression of cortistatin inversely correlated with liver fibrosis grade in mice and humans with hepatic disorders. Cortistatin-deficient mice showed exacerbated signs of liver damage and fibrosis and increased mortality rates when challenged by hepatotoxic and cholestatic injury. Compared with wild-type mice, non-parenchymal liver cells isolated from cortistatin-deficient mice showed increased presence of cells with activated myofibroblast phenotypes and a differential genetic signature that is indicative of activated hepatic stellate cells and periportal fibroblasts and of myofibroblasts with active contractile apparatus. Cortistatin treatment reversed in vivo and in vitro these exaggerated fibrogenic phenotypes and protected from progression to severe liver fibrosis in response to hepatic injury. Conclusion and Implications: We identify cortistatin as an endogenous molecular brake on liver fibrosis and its deficiency as a potential poor-prognosis marker for chronic hepatic disorders that link with fibrosis. Cortistatin-based therapies emerge as attractive strategies for ameliorating severe hepatic fibrosis of various aetiologies.
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- 2022
10. Caracterización del neuropéptido cortistatina en el envejecimiento fisiológico del sistema neuroinmunitario.
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Serrano Martínez, Ignacio, Castillo-González, Julia, Caro, Marta, Forte-Lago, Irene, González-Rey, Elena, Serrano Martínez, Ignacio, Castillo-González, Julia, Caro, Marta, Forte-Lago, Irene, and González-Rey, Elena
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- 2022
11. El neuropéptido cortistatina: una molécula clave regulando la neuroinflamación y la alteración de la barrera hematoencefálica durante los infartos cerebrales.
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Castillo-González, Julia, Ubago-Rodriguez, Ana, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, González-Rey, Elena, Castillo-González, Julia, Ubago-Rodriguez, Ana, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, and González-Rey, Elena
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- 2022
12. Cortistatin regulates fibrosis and myofibroblast activation in experimental hepatotoxic‐ and cholestatic‐induced liver injury
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Benitez, Raquel, primary, Caro, Marta, additional, Andres‐Leon, Eduardo, additional, O'Valle, Francisco, additional, and Delgado, Mario, additional
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- 2022
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13. Protective Role of Cortistatin in Pulmonary Inflammation and Fibrosis
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Barriga, Margarita, Benitez, Raquel, Ferraz-de-Paula, Viviane, Garcia-Frutos, Marina, Caro, Marta, Robledo, Gema, O’Valle, Francisco4, Campos-Salinas, Jenny, Delgado, Mario, Ministerio de Economía y Competitividad (España), Fundação de Amparo à Pesquisa do Estado de São Paulo, Ministerio de Ciencia, Innovación y Universidades (España), Delgado, Mario, and Delgado, Mario [0000-0003-1893-5982]
- Subjects
Neuropeptide ,Macrophages ,Acute lung injury ,Pulmonary inflammation ,Fibroblasts - Abstract
Background and Purpose Acute lung injury (ALI), acute respiratory distress syndrome (ARDS) and pulmonary fibrosis remain major causes of morbidity, mortality and healthcare burden in the critically ill patient. There is an urgent medical need for identifying factors of susceptibility and prognosis and for designing new therapeutic tools for treating these disorders. Here, we evaluate the capacity of the immunomodulatory neuropeptide cortistatin to regulate pulmonary inflammation and fibrosis in vivo. Experimental Approach ALI/ARDS and pulmonary fibrosis were induced experimentally in wild-type and cortistatin-deficient mice by pulmonary infusion of the bacterial endotoxin LPS or the chemotherapeutic drug bleomycin, and the histopathological signs, pulmonary leukocyte infiltration and cytokines and fibrotic markers were evaluated. Key Results Partially-deficient mice in cortistatin showed exacerbated pulmonary damage, pulmonary inflammation, alveolar oedema and fibrosis, and subsequent increased respiratory failure and mortality when challenged to LPS or bleomycin, even at low doses. Treatment with cortistatin reversed these aggravated phenotypes and protected from progression to severe ARDS and fibrosis after high-exposition to both injury agents. Moreover, cortistatin-deficient pulmonary macrophages and fibroblasts showed exaggerated ex vivo inflammatory and fibrotic responses, and treatment with cortistatin impaired their activation. Finally, the protective effects of cortistatin in ALI and pulmonary fibrosis were partially inhibited by specific antagonists for somatostatin- and ghrelin-receptors. Conclusion and Implications We identify to cortistatin as an endogenous break of pulmonary inflammation and fibrosis. Deficiency in cortistatin could be a marker of poor-prognosis in inflammatory/fibrotic pulmonary disorders. Cortistatin-based therapies emerge as attractive candidates to treat severe ALI/ARDS, including SARS-Cov-2-associated ARDS., This study was mainly supported by the Spanish Ministry of Science and Innovation (MICINN, grant SAF2015-67787-R). R.B. was recipient of FPI fellowship from Spanish Ministry of Science and Innovation and M.G.-F. was recipient of FPU fellowship from Spanish Ministry of Universities.V.F-P. was recipient of postdoctoral fellowship from Fundação de Amparo à Pesquisa do Estado de São Paulo - FAPESP (12/21767-5)
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- 2021
14. Neuropeptide Cortistatin Regulates Dermal and Pulmonary Fibrosis in an Experimental Model of Systemic Sclerosis
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Barriga, Margarita, primary, Benitez, Raquel, additional, Robledo, Gema, additional, Caro, Marta, additional, O’Valle, Francisco, additional, Campos-Salinas, Jenny, additional, and Delgado, Mario, additional
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- 2021
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15. Protective role of cortistatin in pulmonary inflammation and fibrosis
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Barriga, Margarita, primary, Benitez, Raquel, additional, Ferraz‐de‐Paula, Viviane, additional, Garcia‐Frutos, Marina, additional, Caro, Marta, additional, Robledo, Gema, additional, O'Valle, Francisco, additional, Campos‐Salinas, Jenny, additional, and Delgado, Mario, additional
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- 2021
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16. Neuropeptide Cortistatin Regulates Dermal and Pulmonary Fibrosis in an Experimental Model of Systemic Sclerosis.
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Barriga, Margarita, Benitez, Raquel, Robledo, Gema, Caro, Marta, O'Valle, Francisco, Campos-Salinas, Jenny, and Delgado, Mario
- Subjects
SYSTEMIC scleroderma ,SCLERODERMA (Disease) ,PULMONARY fibrosis ,CONNECTIVE tissue growth factor ,INTRADERMAL injections ,DIFFERENTIAL forms - Abstract
Introduction: Scleroderma, or systemic sclerosis, is a complex connective tissue disorder characterized by autoimmunity, vasculopathy, and progressive fibrosis of the skin and internal organs. Because its aetiology is unknown, the identification of genes/factors involved in disease severity, differential clinical forms, and associated complications is critical for understanding its pathogenesis and designing novel treatments. Neuroendocrine mediators in the skin emerge as potential candidates. We investigated the role played by the neuropeptide cortistatin in a preclinical model of scleroderma. Methods: Dermal fibrosis was induced by repetitive intradermal injections of bleomycin in wild-type and cortistatin-deficient mice. The histopathological signs and expression of fibrotic markers were evaluated in the skin and lungs. Results: An inverse correlation between cortistatin levels and fibrogenic activation exists in the damaged skin and dermal fibroblasts. Bleomycin-challenged skin lesions of mice that are partially and totally deficient in cortistatin showed exacerbated histopathological signs of scleroderma, characterized by thicker and more fibrotic dermal layer, enlarged epidermis, and increased inflammatory infiltration in comparison to those of wild-type mice. Cortistatin deficiency enhanced dermal collagen deposits, connective tissue growth factor expression, loss of microvessels, and predisposition to suffer severe complications that co-occur with dermal exposition to bleomycin, including pulmonary fibrotic disease and increased mortality. Treatment with cortistatin mitigated these pathological processes. Discussion/Conclusion: We identify cortistatin as an endogenous break of skin inflammation and fibrosis. Deficiency in cortistatin could be a marker of poor prognosis of scleroderma and associated complications. Cortistatin-based therapies emerge as attractive candidates to treat severe forms of systemic sclerosis and to manage fibrosis-related side effects of bleomycin chemotherapy in oncologic patients. [ABSTRACT FROM AUTHOR]
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- 2022
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17. Mesenchymal Stem Cells Induce the Ramification of Microglia Via the Small RhoGTPases Cdc42 and Rac1
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Neubrand, Veronika E., Pedreño, Marta, Caro, Marta, Forte-Lago, Irene, Delgado, Mario, and Gonzalez-Rey, Elena
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- 2014
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18. CORTISTATIN REGULATES FIBROSIS AND MYOFIBROBLAST ACTIVATION IN EXPERIMENTAL HEPATOTOXIC- AND CHOLESTATIC-INDUCED LIVER INJURY
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Benitez, Raquel, primary, Caro, Marta, additional, Andrés-León, Eduardo, additional, O'Valle, Francisco, additional, and Delgado, Mario, additional
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- 2021
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19. The Neuropeptide Cortistatin Alleviates Neuropathic Pain in Experimental Models of Peripheral Nerve Injury
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Falo, Clara P., primary, Benitez, Raquel, additional, Caro, Marta, additional, Morell, Maria, additional, Forte-Lago, Irene, additional, Hernandez-Cortes, Pedro, additional, Sanchez-Gonzalez, Clara, additional, O’Valle, Francisco, additional, Delgado, Mario, additional, and Gonzalez-Rey, Elena, additional
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- 2021
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20. Protective Role of Cortistatin in Pulmonary Inflammation and Fibrosis
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Ministerio de Economía y Competitividad (España), Fundação de Amparo à Pesquisa do Estado de São Paulo, Ministerio de Ciencia, Innovación y Universidades (España), Delgado, Mario [0000-0003-1893-5982], Barriga, Margarita, Benitez, Raquel, Ferraz-de-Paula, Viviane, Garcia-Frutos, Marina, Caro, Marta, Robledo, Gema, O’Valle, Francisco, Campos-Salinas, Jenny, Delgado, Mario, Ministerio de Economía y Competitividad (España), Fundação de Amparo à Pesquisa do Estado de São Paulo, Ministerio de Ciencia, Innovación y Universidades (España), Delgado, Mario [0000-0003-1893-5982], Barriga, Margarita, Benitez, Raquel, Ferraz-de-Paula, Viviane, Garcia-Frutos, Marina, Caro, Marta, Robledo, Gema, O’Valle, Francisco, Campos-Salinas, Jenny, and Delgado, Mario
- Abstract
Background and Purpose Acute lung injury (ALI), acute respiratory distress syndrome (ARDS) and pulmonary fibrosis remain major causes of morbidity, mortality and healthcare burden in the critically ill patient. There is an urgent medical need for identifying factors of susceptibility and prognosis and for designing new therapeutic tools for treating these disorders. Here, we evaluate the capacity of the immunomodulatory neuropeptide cortistatin to regulate pulmonary inflammation and fibrosis in vivo. Experimental Approach ALI/ARDS and pulmonary fibrosis were induced experimentally in wild-type and cortistatin-deficient mice by pulmonary infusion of the bacterial endotoxin LPS or the chemotherapeutic drug bleomycin, and the histopathological signs, pulmonary leukocyte infiltration and cytokines and fibrotic markers were evaluated. Key Results Partially-deficient mice in cortistatin showed exacerbated pulmonary damage, pulmonary inflammation, alveolar oedema and fibrosis, and subsequent increased respiratory failure and mortality when challenged to LPS or bleomycin, even at low doses. Treatment with cortistatin reversed these aggravated phenotypes and protected from progression to severe ARDS and fibrosis after high-exposition to both injury agents. Moreover, cortistatin-deficient pulmonary macrophages and fibroblasts showed exaggerated ex vivo inflammatory and fibrotic responses, and treatment with cortistatin impaired their activation. Finally, the protective effects of cortistatin in ALI and pulmonary fibrosis were partially inhibited by specific antagonists for somatostatin- and ghrelin-receptors. Conclusion and Implications We identify to cortistatin as an endogenous break of pulmonary inflammation and fibrosis. Deficiency in cortistatin could be a marker of poor-prognosis in inflammatory/fibrotic pulmonary disorders. Cortistatin-based therapies emerge as attractive candidates to treat severe ALI/ARDS, including SARS-Cov-2-associated ARDS.
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- 2021
21. Involvement of the neuropeptide cortistatin in neuroinflammation and blood-brain barrier dysfunction in ischemic stroke.
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Castillo-González, Julia, Ubago-Rodriguez, Ana, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, González-Rey, Elena, Castillo-González, Julia, Ubago-Rodriguez, Ana, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, and González-Rey, Elena
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- 2021
22. Role of the neuropeptide cortistatin in neuro-immune dysregulation and blood-brain barrier dysfunction during ischemic stroke.
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Castillo-González, Julia, Ubago-Rodríguez, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, González-Rey, Elena, Castillo-González, Julia, Ubago-Rodríguez, Caro, Marta, Forte-Lago, Irene, Buscemi, Lara, Hernández-Cortés, Pedro, Hirt, Lorenz, and González-Rey, Elena
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- 2021
23. Analysis of the molecular and functional roles of cortistatin on the dynamics of oligodendrocyte generation and myelination.
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González-Rey, Elena, Castillo-González, Julia, Forte-Lago, Irene, Caro, Marta, Andrés-León, Eduardo, O'Valle, Francisco, Falo, CP, González-Rey, Elena, Castillo-González, Julia, Forte-Lago, Irene, Caro, Marta, Andrés-León, Eduardo, O'Valle, Francisco, and Falo, CP
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- 2021
24. Cortistatin: a key factor involved in the molecular and cellular mechanisms of the healthy aging.
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Serrano-Martínez, Ignacio, Castillo-González, Julia, Caro, Marta, Forte-Lago, Irene, González-Rey, Elena, Serrano-Martínez, Ignacio, Castillo-González, Julia, Caro, Marta, Forte-Lago, Irene, and González-Rey, Elena
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- 2021
25. THE NEUROPEPTIDE CORTISTATIN REGULATES THE PROGRAMMING OF BRAIN ENDOTHELIAL CELLS UNDER PHYSIOLOGICAL AND PATHOLOGICAL CONDITIONS
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Ruiz, José, Serrano-Martínez, Ignacio, Forte-Lago, Irene, Ubago-Rodríguez, Ana, Caro, Marta, Pérez-Gómez, Jesús, Andrés-León, Eduardo, Sánchez-Navarro, Macarena, Luque, Raúl, and Castillo-González, Julia
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- 2023
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26. THE NEUROPEPTIDE CORTISTATIN, A CRUCIAL MODULATOR IN THE IMMUNE DYSREGULATION AND BLOOD-BRAIN BARRIER DYSFUNCTION UNDERLYING ISCHEMIC BRAIN INJURY
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Buscemi, Lara, Martínez, Ignacio Serrano, Lago, Irene Forte, Caro, Marta, Cortés, Pedro Hernández, Hirt, Lorenz, and Gonzalez-Rey, Elena
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- 2023
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27. An international registry for emergent pathogens and pregnancy
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Alice Panchaud, Guillaume Favre, Leo Pomar, Manon Vouga, Karoline Aebi-Popp, David Baud, Tallarek Ann-Christin, Strizek Brigitte, Hecher Kurt, Böckenhoff Paul, Schrey-Petersen Susanne, Mullins Edward, Bromley Rebecca, Whitehead Clare, Rolnik Daniel, Deprest Jan, Richter Jute, Gomes Luz Adriana, Bohrer Betania, Carvalho Ribeiro-do-Valle Carolina, Garanhani Surita Fernanda, Schuler-Faccini Lavinia, Osorio Wender Maria Celeste, Da Rocha Oppermann Maria Lucia, Moreira de sa Renato Augusto, Quintana Silvana, Sjaus Ana, Rahman Arifa, Hamel-Thibault Audrey, Nash Christopher, Kakkar Fatima, Berger Howard, Boucoiran Isabelle, Pasquier Jean-Charles, Snelgrove John, Zipursky Jonathan, Lacroix Meagan, Whittle Wendy, Fuenzalida Javiera, Carvajal Jorge, Guerra Canales Manuel, Hernandez Olivia, Yin Mingzhu, Chen Xiang, Qi Xiaolong, Sanín Blair José Enrique, Gonzalez Ricardo, Cano Aguilar Africa, Rodriguez Vicente Agueda, Tubau Navarra Albert, Puertas Prieto Alberto, Cano Garcia Alejandra Maria, Carrascal Cumplido Ana, Villalba Yarza Ana, Filloy Lavia Ana Cristina, Fernandez Alonso Ana Maria, Sanchez Vegazo Garcia Angeles, Goncé Anna, Ruano Garcia Antonio, Sanchez Munoz Antonio, Marcos Puig Beatriz, Munoz Abellana Begona, Garrido Luque Belen, Fernandez Fernandez Camino, Larranaga Azcarate Carlos, Baena Luque Carmen, Orizales Lago Carmen Maria, Alvarez Colomo Cristina, Lesmes Heredia Cristina, Ruiz Aguilar Cristina, Ferriols Perez Elena, Pascual Salvador Elena, Carmona Sanchez Encarnacion, Alvarez Silvares Esther, Canedo Carballeira Esther Maria, Moran Antolin Eva, Muelas Parraga Eva Maria, Oviedo Perez Eva Maria, Gonzalez Carvajal Francisco Jesus, Agudo Iène, Ocerin Bengoa Iratxe, Gastaca Abasolo Irene, Cabello de Alba Fernandez Isabel, Alvarez Javier, Duro Gomez Jorge, Atxotegi Jose, Navarrina Martinez José, Ruiz Aragon José, Sainz Bueno José Antonio, Adanez Garcia Jose Manuel, Broullon Molanes José Roman, Wizner de Alva Juan Carlos, Forcen Acebal Laura, Gonzalez Rodriguez Laura, Aceituno Velasco Longinos, Cerrillos Gonzalez Lucas, Trigo Lucas, Diaz Meca Lucia, Parada Millan M Carmen, Molina Oller Magdalena, Dominguez Gonzalez Manuel, Munoz Chapuli Gutierrez Mar, Caridad Ortiz Herrera Maria, Nieves Quesada Fernandez Maria, Suarez Arana Maria, Teulon Gonzalez Maria, Zafra Bailera Maria, Duenas Carazo Maria Begona, Gonzalez Macias Maria Carmen, Pilar Guadix Martin Maria del, Barbancho Lopez Maria del Carmen, Medina Mallen Maria del Carmen, Pardo Pumar Maria Isabel, Gimeno Gimeno Maria Joaquina, Nunez Valera Maria José, Pelegay Escartin Maria José, Camacho Caro Marta, Garcia Sanchez Marta, Meca Casbas Marta Ruth, Fraca Padilla Mercedes, Ramirez Gomez Mercedes, Catalina Coello Monica, Cruz Lemini Monica, Perez Perez Noelia, Nieto Velasco Olga, Alomar Mateu Onofre, Martinez Perez Oscar, Vaquerizo Ruiz Oscar, Barrio Fernández Pablo Guillermo del, Monteliu Gonzalez Pilar, Prats Rodriguez Pilar, Vivaracho Terrer Porfirio, Gonzales Seoane Raquel, Jimenez Velazquez Raquel, Alvarez Fernandez Rebeca, Lopez Perez Rocio, Ostos Serna Rosa Maria, Redondo Aguilar Rosario, Bernardo Vega Rut, Cano Sandra, Mateos Lopez Silvia, Fernandez Garcia Susana, Soldevilla Perez Susana, Manrique Gomez Tania, Munoz Carmona Vitor, Ko Albert I, Johnson Anthony, Nielsen Saines Karin, Cambou Mary, Grechukhina Olga, Neupane Sahara, Reddy Uma, Shah Zubin, Breton Bénédicte, Garabedian Charles, Bertholdt Charline, Poncelet Christophe, Subtil Damien, Musso Didier, Henry Estelle, Plantefeve Gaetan, Ducarme Guillaume, Pelerin Helene, Dimet Jerome, Cottin Judith, Stiremann Julien, Lambert Véronique, Hcini Najeh, Salomon Laurent, Sentilhes Loïc, Giral Marylene, Mottet Nicolas, Morel Olivier, Rozenberg Patrick, Lucie Sedille, Quibel Thibaud, Karagianni Vasiliki, Equy Véronique, Ville Yves, Carles Gabriel, Ruehl Ina, Cleary Brian, Malone Fergal, Higgins Mary, Geary Michael, Hadar Eran, Malinger Gustavo, Sela Hen, Krajden Haratz Karina, Maymon Ron, Yogev Yariv, De Luca Carmen, De Santis Marco, Rosso Telefono, Atallah David, Boguziene Emilija, Germes Pina Fernando, Van den Akker Thomas, Gil-Guevara Enrique, Marchena Jeannette, Ventura Walter, Pereira Alcides, Ayres de Campos Diogo, Charepe Nadia, Viana Pinto Pedro, Ntasumbumuyange Diomede, Rulisa Stephen, Panchaud Alice, Radan Anda-Petronela, Papadia Andrea, Bloch Andrea, Feki Anis, Muller Brochut Anne-Claude, Toussaint Arnaud, Eggel-Hort Béatrice, Martinez de Tejada Begoña, Frey Tirri Brigitte, Weber Brigitte, Blume Carolin, Monod Cécile, Kahlert Christian, Voekt Cora, Surbek Daniel, Baud David, Bassler Dirk, Mueller Doris, Prentl Elke Barbara, Gerber Eva, Rothe Friederike, Eric Giannoni, Favre Guillaume, Hoesli Irene, Mathis Jérôme, Lepigeon Karine, Aebi-Popp Karoline, Pomar Leo, Schäffer Leonhard, Raio Luigi, Vouga Manon, Huesler Charles Margaret, Rossier Marie-Claude, Hodel Markus, Kaufmann Martin, Gavillet Mathilde, Boulvain Michel, Todesco Bernasconi Monya, Bickle Myriam, Ochsenbein Kölble Nicole, Jarrah Omar, Kanellos Panagiotis, Brasier Lutz Pascale, Capoccia Brugger Romina, Heldstab Sandra, Heldstab Sandra Andrea, Rouiller Cornu Sylvie, Fischer Tina, Winterfeld Ursula, Lambelet Valentine, Rieder Wawrzyniec, Greub Gilbert, Gengler Carole, Patel Rena C, Huespe Miguel Angel, Nieto-Calvache Albaro José, COVI-Preg group, Ann-Christin, T., Brigitte, S., Kurt, H., Paul, B., Susanne, S.P., Edward, M., Rebecca, B., Clare, W., Daniel, R., Jan, D., Jute, R., Adriana, G.L., Betania, B., Carolina, C.R., Fernanda, G.S., Lavinia, S.F., Maria Celeste, O.W., Maria Lucia, DRO, Renato Augusto, M.S., Silvana, Q., Ana, S., Arifa, R., Audrey, H.T., Christopher, N., Fatima, K., Howard, B., Isabelle, B., Jean-Charles, P., John, S., Jonathan, Z., Meagan, L., Wendy, W., Javiera, F., Jorge, C., Manuel, G.C., Olivia, H., Mingzhu, Y., Xiang, C., Xiaolong, Q., José Enrique, S.B., Ricardo, G., Africa, C.A., Agueda, R.V., Albert, T.N., Alberto, P.P., Alejandra Maria, C.G., Ana, C.C., Ana, V.Y., Ana Cristina, F.L., Ana Maria, F.A., Angeles, SVG, Anna, G., Antonio, R.G., Antonio, S.M., Beatriz, M.P., Begona, M.A., Belen, G.L., Camino, F.F., Carlos, L.A., Carmen, B.L., Carmen Maria, O.L., Cristina, A.C., Cristina, L.H., Cristina, R.A., Elena, F.P., Elena, P.S., Encarnacion, C.S., Esther, A.S., Esther Maria, C.C., Eva, M.A., Eva Maria, M.P., Eva Maria, O.P., Francisco Jesus, G.C., Iène, A., Iratxe, O.B., Irene, G.A., Isabel, CAF, Javier, A., Jorge, D.G., Jose, A., José, N.M., José, R.A., José Antonio, S.B., Jose Manuel, A.G., José Roman, B.M., Juan Carlos, W.A., Laura, F.A., Laura, G.R., Longinos, A.V., Lucas, C.G., Lucas, T., Lucia, D.M., M Carmen, P.M., Magdalena, M.O., Manuel, D.G., Mar, MCG, Maria, COH, Maria, NQF, Maria, S.A., Maria, T.G., Maria, Z.B., Maria Begona, D.C., Maria Carmen, G.M., Maria Del, PGM, Maria Del Carmen, B.L., Maria Del Carmen, M.M., Maria Isabel, P.P., Maria Joaquina, G.G., Maria José, N.V., Maria José, P.E., Marta, C.C., Marta, G.S., Marta Ruth, M.C., Mercedes, F.P., Mercedes, R.G., Monica, C.C., Monica, C.L., Noelia, P.P., Olga, N.V., Onofre, A.M., Oscar, M.P., Oscar, V.R., Pablo Guillermo Del, B.F., Pilar, M.G., Pilar, P.R., Porfirio, V.T., Raquel, G.S., Raquel, J.V., Rebeca, A.F., Rocio, L.P., Rosa Maria, O.S., Rosario, R.A., Rut, B.V., Sandra, C., Silvia, M.L., Susana, F.G., Susana, S.P., Tania, M.G., Vitor, M.C., Albert I, K., Anthony, J., Karin, N.S., Mary, C., Olga, G., Sahara, N., Uma, R., Zubin, S., Bénédicte, B., Charles, G., Charline, B., Christophe, P., Damien, S., Didier, M., Estelle, H., Gaetan, P., Guillaume, D., Helene, P., Jerome, D., Judith, C., Julien, S., Véronique, L., Najeh, H., Laurent, S., Loïc, S., Marylene, G., Nicolas, M., Olivier, M., Patrick, R., Sedille, L., Thibaud, Q., Vasiliki, K., Véronique, E., Yves, V., Gabriel, C., Ina, R., Brian, C., Fergal, M., Mary, H., Michael, G., Eran, H., Gustavo, M., Hen, S., Karina, K.H., Ron, M., Yariv, Y., Carmen, L., Marco, S., Telefono, R., David, A., Emilija, B., Fernando, G.P., Thomas, VDA, Enrique, G.G., Jeannette, M., Walter, V., Alcides, P., Diogo, A.C., Nadia, C., Pedro, V.P., Diomede, N., Stephen, R., Alice, P., Anda-Petronela, R., Andrea, P., Andrea, B., Anis, F., Anne-Claude, M.B., Arnaud, T., Béatrice, E.H., Begoña, M.T., Brigitte, F.T., Brigitte, W., Carolin, B., Cécile, M., Christian, K., Cora, V., Daniel, S., David, B., Dirk, B., Doris, M., Elke Barbara, P., Eva, G., Friederike, R., Giannoni, E., Guillaume, F., Irene, H., Jérôme, M., Karine, L., Karoline, A.P., Leo, P., Leonhard, S., Luigi, R., Manon, V., Margaret, H.C., Marie-Claude, R., Markus, H., Martin, K., Mathilde, G., Michel, B., Monya, T.B., Myriam, B., Nicole, O.K., Omar, J., Panagiotis, K., Pascale, B.L., Romina, C.B., Sandra, H., Sandra Andrea, H., Sylvie, R.C., Tina, F., Ursula, W., Valentine, L., Wawrzyniec, R., Gilbert, G., Carole, G., Rena C, P., Miguel Angel, H., and Albaro José, N.C.
- Subjects
Diagnostic Screening Programs ,medicine.medical_specialty ,2019-20 coronavirus outbreak ,Coronavirus disease 2019 (COVID-19) ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,Pneumonia, Viral ,Severe Acute Respiratory Syndrome ,Communicable Diseases, Emerging ,Risk Assessment ,Betacoronavirus ,Fetus ,Pregnancy ,Risk Factors ,Pandemic ,medicine ,Humans ,Registries ,610 Medicine & health ,Intensive care medicine ,Pandemics ,Zika Virus Infection ,Viral Epidemiology ,business.industry ,Pregnancy Outcome ,Betacoronavirus/growth & development ,Betacoronavirus/immunology ,Communicable Diseases, Emerging/epidemiology ,Communicable Diseases, Emerging/prevention & control ,Coronavirus Infections/epidemiology ,Diagnostic Screening Programs/standards ,Female ,Interdisciplinary Placement/methods ,Pneumonia, Viral/epidemiology ,Pregnancy Outcome/epidemiology ,Severe Acute Respiratory Syndrome/epidemiology ,Zika Virus/immunology ,Zika Virus Infection/epidemiology ,COVID-19 ,Zika Virus ,General Medicine ,medicine.disease ,Interdisciplinary Placement ,sars-cov-2 ,Settore MED/40 - GINECOLOGIA E OSTETRICIA ,Coronavirus Infections ,business - Published
- 2020
28. Adipose-derived mesenchymal stromal cells induce immunomodulatory macrophages which protect from experimental colitis and sepsis
- Author
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Anderson, Per, Souza-Moreira, Luciana, Morell, Maria, Caro, Marta, OʼValle, Francisco, Gonzalez-Rey, Elena, and Delgado, Mario
- Published
- 2013
- Full Text
- View/download PDF
29. Analgesic Effect of the Neuropeptide Cortistatin in Murine Models of Arthritic Inflammatory Pain
- Author
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Morell, Maria, Souza-Moreira, Luciana, Caro, Marta, OʼValle, Francisco, Forte-Lago, Irene, de Lecea, Luis, Gonzalez-Rey, Elena, and Delgado, Mario
- Published
- 2013
- Full Text
- View/download PDF
30. Genetic association of vasoactive intestinal peptide receptor with rheumatoid arthritis: Altered expression and signal in immune cells
- Author
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Delgado, Mario, Robledo, Gema, Rueda, Blanca, Varela, Nieves, OʼValle, Francisco, Hernandez-Cortes, Pedro, Caro, Marta, Orozco, Gisela, Gonzalez-Rey, Elena, and Martin, Javier
- Published
- 2008
31. Vasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses
- Author
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Ministerio de Economía y Competitividad (España), Junta de Andalucía, Benitez, Raquel [0000-0002-0773-108X], Durán-Prado, M. [0000-0001-9652-5765], O'Valle, Francisco [0000-0001-9207-2287], González-Rey, Elena [0000-0003-3917-9020], Delgado, M. [0000-0003-1893-5982], Benitez, Raquel, Delgado-Maroto, V., Caro, Marta, Forte-Lago, Irene, Durán-Prado, Mario, O'Valle, Francisco, Lichtman, Andrew H., González-Rey, Elena, Delgado, M., Ministerio de Economía y Competitividad (España), Junta de Andalucía, Benitez, Raquel [0000-0002-0773-108X], Durán-Prado, M. [0000-0001-9652-5765], O'Valle, Francisco [0000-0001-9207-2287], González-Rey, Elena [0000-0003-3917-9020], Delgado, M. [0000-0003-1893-5982], Benitez, Raquel, Delgado-Maroto, V., Caro, Marta, Forte-Lago, Irene, Durán-Prado, Mario, O'Valle, Francisco, Lichtman, Andrew H., González-Rey, Elena, and Delgado, M.
- Abstract
Vasoactive intestinal peptide (VIP) is a neuropeptide that exerts various vascular and cardioprotective functions and regulates immune function and inflammatory response at multiple levels. However, its role in inflammatory cardiovascular disorders is largely unknown. Myocarditis and atherosclerosis are two inflammatory and autoimmune cardiovascular diseases that cause important adverse circulatory events. In this study, we investigate the therapeutic effects of VIP in various well-established preclinical models of experimental autoimmune myocarditis and atherosclerosis. Intraperitoneal injection of VIP during the effector phase of experimental autoimmune myocarditis in susceptible BALB/c mice significantly reduced its prevalence, ameliorated signs of heart hypertrophy and injury, attenuated myocardial inflammatory infiltration, and avoided subsequent profibrotic cardiac remodeling. This effect was accompanied by a reduction of Th17-driven cardiomyogenic responses in peripheral lymphoid organs and in the levels of myocardial autoantibodies. In contrast, acute and chronic atherosclerosis was induced in apolipoprotein E-deficient mice fed a hyperlipidemic diet and subjected to partial carotid ligation. Systemic VIP treatment reduced the number and size of atherosclerotic plaques in carotid, aorta, and sinus in hypercholesterolemic mice. VIP reduced Th1-driven inflammatory responses and increased regulatory T cells in atherosclerotic arteries and their draining lymph nodes. VIP also regulated cholesterol efflux in macrophages and reduced the formation of foam cells and their presence in atherosclerotic plaques. Finally, VIP inhibited proliferation and migration of smooth muscle cells and neointima formation in a mouse model of complete carotid ligation. These findings encourage further studies aimed to assess whether VIP can be used as a pharmaceutical agent to treat heart inflammation and atherosclerosis.
- Published
- 2018
32. The atypical RhoGTPase RhoE/Rnd3 is a key molecule to acquire a neuroprotective phenotype in microglia
- Author
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Michael J. Fox Foundation for Parkinson's Research, Junta de Andalucía, Neubrand, Veronika E., Forte-Lago, Irene, Caro, Marta, Delgado, M., Michael J. Fox Foundation for Parkinson's Research, Junta de Andalucía, Neubrand, Veronika E., Forte-Lago, Irene, Caro, Marta, and Delgado, M.
- Abstract
[Background] Over-activated microglia play a central role during neuroinflammation, leading to neuronal cell death and neurodegeneration. Reversion of over-activated to neuroprotective microglia phenotype could regenerate a healthy CNS-supporting microglia environment. Our aim was to identify a dataset of intracellular molecules in primary microglia that play a role in the transition of microglia to a ramified, neuroprotective phenotype., [Methods] We exploited the anti-inflammatory and neuroprotective properties of conditioned medium of adipose-derived mesenchymal stem cells (CM) as a tool to generate the neuroprotective phenotype of microglia in vitro, and we set up a microscopy-based siRNA screen to identify its hits by cell morphology., [Results] We initially assayed an array of 157 siRNAs against genes that codify proteins and factors of cytoskeleton and activation/inflammatory pathways in microglia. From them, 45 siRNAs significantly inhibited the CM-induced transition from a neurotoxic to a neuroprotective phenotype of microglia, and 50 siRNAs had the opposite effect. As a proof-of-concept, ten of these targets were validated with individual siRNAs and by downregulation of protein expression. This validation step resulted essential, because three of the potential targets were false positives. The seven validated targets were assayed in a functional screen that revealed that the atypical RhoGTPase RhoE/Rnd3 is necessary for BDNF expression and plays an essential role in controlling microglial migration., [Conclusions] Besides the identification of RhoE/Rnd3 as a novel inducer of a potential neuroprotective phenotype in microglia, we propose a list of potential targets to be further confirmed with selective activators or inhibitors.
- Published
- 2018
33. Vasoactive Intestinal Peptide Ameliorates Acute Myocarditis and Atherosclerosis by Regulating Inflammatory and Autoimmune Responses
- Author
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Benitez, Raquel, primary, Delgado-Maroto, Virginia, additional, Caro, Marta, additional, Forte-Lago, Irene, additional, Duran-Prado, Mario, additional, O’Valle, Francisco, additional, Lichtman, Andrew H., additional, Gonzalez-Rey, Elena, additional, and Delgado, Mario, additional
- Published
- 2018
- Full Text
- View/download PDF
34. Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features
- Author
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Magatti, Marta, Vertua, Elsa, De Munari, Silvia, Caro, Marta, Caruso, Maddalena, Silini, Antonietta, Delgado, Mario, Parolini, Ornella, Parolini, Ornella (ORCID:0000-0002-5211-6430), Magatti, Marta, Vertua, Elsa, De Munari, Silvia, Caro, Marta, Caruso, Maddalena, Silini, Antonietta, Delgado, Mario, Parolini, Ornella, and Parolini, Ornella (ORCID:0000-0002-5211-6430)
- Abstract
Human amniotic mesenchymal cells (hAMTCs) possess interesting immunomodulatory properties, making them attractive candidates for regenerative medicine applications. Recent in vivo reports argue in favour of an important role for macrophages as targets of hAMTC-mediated suppression of inflammation and the enhancement of tissue repair. However, a comprehensive study of the effects of hAMTCs and their conditioned medium (CM) on human macrophage differentiation and function is unavailable. In the present study we found that hAMTCs and CM induce the differentiation of myeloid cells (U937 and monocytes) towards macrophages. We then investigated their effects on monocytes differentiated toward pro-inflammatory M1 and anti-inflammatory M2 macrophages. Monocytes treated under M1 conditions in the presence of hAMTCs or CMs shifted towards M2-like macrophages, which expressed CD14, CD209, CD23, CD163 and PM-2 K, possessed higher phagocytic activity and produced higher IL-10 and lower pro-inflammatory cytokines. They were also poor T cell stimulators and Th1 inducers, while they were able to increase activated and naïve suppressive Treg subsets. We show that prostaglandins, and not IL-6, play a role in determining the M2 activation status. Instead, monocytes treated under M2 conditions in the presence of hAMTCs or CM retained M2-like features, but with an enhanced anti-inflammatory profile, having a reduced expression of the co-stimulatory molecule CD80, reduced phagocytosis activity and decreased the secretion of inflammatory chemokines. Importantly, we provide evidence that macrophages re-educated by CM improve tissue regeneration/repair in wound-healing models. In conclusion, we identified new cell targets of hAMTCs and their bioactive factors and here provide insight into the beneficial effects observed when these cells are used in therapeutic approaches in vivo.
- Published
- 2017
35. Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features
- Author
-
Magatti, Marta, Vertua, Elsa, De Munari, Silvia, Caro, Marta, Caruso, Maddalena, Silini, Antonietta, Delgado, M., Parolini, Ornella, Delgado, M. [0000-0003-1893-5982], and Delgado, M.
- Subjects
M1 and M2 macrophages ,conditioned medium ,human amnion ,immunomodulation ,mesenchymal stem/stromal cells ,monocyte ,regenerative medicine ,wound healing ,T-Lymphocytes ,Human amnion ,Wound healing ,Monocyte ,Monocytes ,Immunomodulation ,Phagocytosis ,Animals ,Humans ,Regeneration ,Settore BIO/13 - BIOLOGIA APPLICATA ,Amnion ,Conditioned medium ,Research Articles ,Cell Proliferation ,Mesenchymal stem/stromal cells ,Interleukin-6 ,Macrophages ,Cell Polarity ,Cell Differentiation ,U937 Cells ,Mice, Inbred C57BL ,Phenotype ,Culture Media, Conditioned ,Regenerative medicine ,Prostaglandins ,Research Article - Abstract
Human amniotic mesenchymal cells (hAMTCs) possess interesting immunomodulatory properties, making them attractive candidates for regenerative medicine applications. Recent in vivo reports argue in favour of an important role for macrophages as targets of hAMTC-mediated suppression of inflammation and the enhancement of tissue repair. However, a comprehensive study of the effects of hAMTCs and their conditioned medium (CM) on human macrophage differentiation and function is unavailable. In the present study we found that hAMTCs and CM induce the differentiation of myeloid cells (U937 and monocytes) towards macrophages. We then investigated their effects on monocytes differentiated toward pro-inflammatory M1 and anti-inflammatory M2 macrophages. Monocytes treated under M1 conditions in the presence of hAMTCs or CMs shifted towards M2-like macrophages, which expressed CD14, CD209, CD23, CD163 and PM-2 K, possessed higher phagocytic activity and produced higher IL-10 and lower pro-inflammatory cytokines. They were also poor T cell stimulators and Th1 inducers, while they were able to increase activated and naïve suppressive Treg subsets. We show that prostaglandins, and not IL-6, play a role in determining the M2 activation status. Instead, monocytes treated under M2 conditions in the presence of hAMTCs or CM retained M2-like features, but with an enhanced anti-inflammatory profile, having a reduced expression of the co-stimulatory molecule CD80, reduced phagocytosis activity and decreased the secretion of inflammatory chemokines. Importantly, we provide evidence that macrophages re-educated by CM improve tissue regeneration/repair in wound-healing models. In conclusion, we identified new cell targets of hAMTCs and their bioactive factors and here provide insight into the beneficial effects observed when these cells are used in therapeutic approaches in vivo., The authors wish to thank the physicians and midwives of theDepartment of Obstetrics and Gynaecology of FondazionePoliambulanza–Istituto Ospedaliero (Brescia, Italy) and all themothers who donated placentae; the personnel of the Depart-ment of Radiation Oncology of Fondazione Poliambulanza–Istituto Ospedaliero (Brescia, Italy) for assistance with cell irradi-ation; and the Centre of Immune Transfusion of Spedali Civili(Brescia, Italy), who provided buffy coats. This study was sup-ported by Fondazione Poliambulanza–Istituto Ospedaliero, theCariplo Foundation (Grant Nos 2011-0495 and 2012-0842), theItalian Ministry of Health project‘Ricerca Finalizzata’(ProjectNo. RF-2010-2315681), the Competitiveness ROP ERDF 2007–2013 of Lombardy Region (Regional Operational Programme ofthe European Regional Development Fund–Progetto NUTECNUove TECnologie ID No. 30263049) and the Spanish Ministryof Economy and Competitivenes
- Published
- 2016
36. Anàlisi de les imminents reformes processals i la seva aplicació a Catalunya. Problemàtica pròpia i riscos detectats. Propostes de millora. Cap a un nou model de justícia
- Author
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Pesqueira Caro, Marta, Magariños Yánez, José Alberto, and Centre d'Estudis Jurídics i Formació Especialitzada (Catalunya)
- Subjects
Justícia -- Administració -- Catalunya ,343 - Dret penal. Delictes ,Dret processal penal - Abstract
Per diferents motius, l'acció de la justícia es troba permanentment d'actualitat. Una de les causes és la contínua novetat que prové de les propostes de modernització en els diversos àmbits, que tracten de pal·liar els dèficits amb els quals s'enfronta cada dia l'acció judicial. El debat és ja antic i permanent, sent que, simultàniament un ventall de projectes ha aparegut amb la intenció de dur a terme un canvi profund i determinant en la visió de l'estructura del Poder Judicial i dels serveis associats. En particular, la proposta de reforma de Llei Orgànica del Poder Judicial i de Demarcació i Planta, suposa la concentració de tots els jutjats a les capitals de província, amb el risc d'allunyament enfront dels ciutadans i problemes associats. L'esborrany de Codi Processal Penal aposta per un nou sistema de recerca a càrrec del Ministeri Fiscal, amb curts terminis taxats per a la finalització del procediment, promoció de la mediació i augment de les possibilitats de no continuació de la causa, a més una concentració i simplificació de totes les fases del procediment penal. D'altra banda, el Registre Civil ha estat retirat dels jutjats però, malgrat el transcurs del temps, no s'és capaç d'identificar a quin col·lectiu li correspondrà aquesta funció, amb la conseqüent generació d'una important inquietud social. Aquestes i altres novetats seran analitzades en profunditat, amb especial perspectiva des de l'àmbit de Catalunya, tractant d'aportar solucions i propostes de millora. For various reasons, the judicial action is permanently relevant. One reason is the ongoing innovation that comes from modernization proposals in various areas, aiming to address the deficits facing prosecution every day. The debate is as old and permanent, being that simultaneously a range of projects has appeared with the intention of conducting a thorough and decisive change in the view of the structure of the judiciary and the associated services. In particular, the proposed reform of the Organic Law of Judicial Power and Ground Demarcation, is the concentration of all the courts in the provincial capitals, with the risk away to citizens and associated problems. The draft Criminal Procedure Code advocates a new system of investigation by the Public Prosecutor assessed with short deadlines for the completion of the process, promotion of mediation and increase the chances of not then cause further concentration and simplification all stages of criminal proceedings. Furthermore, the Registry has been removed from the courts but, despite the passage of time, is not able to identify which group will be up this role, with the consequent generation of significant social unrest. These and other developments will be analyzed in depth, with particular perspective within Catalonia, trying to provide solutions and suggestions for improvement. Por diferentes motivos, la acción de la justicia se encuentra permanentemente de actualidad. Una de las causas es la continua novedad que proviene de las propuestas de modernización en los diversos ámbitos, que tratan de paliar los déficits con los que se enfrenta cada día la acción judicial. El debate es ya antiguo y permanente, siendo que, simultáneamente un abanico de proyectos ha aparecido con la intención de llevar a cabo un cambio profundo y determinante en la visión de la estructura del Poder Judicial y de los servicios asociados. En particular, la propuesta de reforma de Ley Orgánica del Poder Judicial y de Demarcación y Planta, supone la concentración de todos los juzgados en las capitales de provincia, con el riesgo de alejamiento frente a los ciudadanos y problemas asociados. El borrador de Código Procesal Penal apuesta por un nuevo sistema de investigación a cargo del Ministerio Fiscal, con cortos plazos tasados para la finalización del procedimiento, promoción de la mediación y aumento de las posibilidades de no continuación de la causa, además una concentración y simplificación de todas las fases del procedimiento penal. Por otro lado, el Registro Civil ha sido retirado de los juzgados pero, a pesar del transcurso del tiempo, no se es capaz de identificar a qué colectivo le corresponderá esa función, con la consecuente generación de una importante inquietud social. Éstas y otras novedades serán analizadas en profundidad, con especial perspectiva desde el ámbito de Cataluña, tratando de aportar soluciones y propuestas de mejora.
- Published
- 2015
37. Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features
- Author
-
Delgado, M. [0000-0003-1893-5982], Magatti, Marta, Vertua, Elsa, De Munari, Silvia, Caro, Marta, Caruso, Maddalena, Silini, Antonietta, Delgado, M., Parolini, Ornella, Delgado, M. [0000-0003-1893-5982], Magatti, Marta, Vertua, Elsa, De Munari, Silvia, Caro, Marta, Caruso, Maddalena, Silini, Antonietta, Delgado, M., and Parolini, Ornella
- Abstract
Human amniotic mesenchymal cells (hAMTCs) possess interesting immunomodulatory properties, making them attractive candidates for regenerative medicine applications. Recent in vivo reports argue in favour of an important role for macrophages as targets of hAMTC-mediated suppression of inflammation and the enhancement of tissue repair. However, a comprehensive study of the effects of hAMTCs and their conditioned medium (CM) on human macrophage differentiation and function is unavailable. In the present study we found that hAMTCs and CM induce the differentiation of myeloid cells (U937 and monocytes) towards macrophages. We then investigated their effects on monocytes differentiated toward pro-inflammatory M1 and anti-inflammatory M2 macrophages. Monocytes treated under M1 conditions in the presence of hAMTCs or CMs shifted towards M2-like macrophages, which expressed CD14, CD209, CD23, CD163 and PM-2 K, possessed higher phagocytic activity and produced higher IL-10 and lower pro-inflammatory cytokines. They were also poor T cell stimulators and Th1 inducers, while they were able to increase activated and naïve suppressive Treg subsets. We show that prostaglandins, and not IL-6, play a role in determining the M2 activation status. Instead, monocytes treated under M2 conditions in the presence of hAMTCs or CM retained M2-like features, but with an enhanced anti-inflammatory profile, having a reduced expression of the co-stimulatory molecule CD80, reduced phagocytosis activity and decreased the secretion of inflammatory chemokines. Importantly, we provide evidence that macrophages re-educated by CM improve tissue regeneration/repair in wound-healing models. In conclusion, we identified new cell targets of hAMTCs and their bioactive factors and here provide insight into the beneficial effects observed when these cells are used in therapeutic approaches in vivo.
- Published
- 2016
38. Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features
- Author
-
Magatti, Marta, primary, Vertua, Elsa, additional, De Munari, Silvia, additional, Caro, Marta, additional, Caruso, Maddalena, additional, Silini, Antonietta, additional, Delgado, Mario, additional, and Parolini, Ornella, additional
- Published
- 2016
- Full Text
- View/download PDF
39. Tratamiento del aborto espontáneo (Médico Vs. Legrado): experiencia en un año en el Hospital Virgen de la Victoria
- Author
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Camacho Caro, Marta, Condor-Muñoz, Luis Miguel, Quesada Hurtado, Josefa, Ríus Díaz, Francisca, Cirugía, Obstetricia y Ginecología, and Rius-Diaz, Francisca
- Subjects
Tratamiento de aborto espontáneo ,Aborto espontáneo - Tratamiento - Tesis doctorales ,Misoprostol - Tesis doctorales ,Legrado ,Misoprostol ,Tesis Doctorales - Abstract
Estudio descriptivo que compara el misoprostol versus legrado para el tratamiento del aborto espontáneo del primer trimestre y demuestra que el tratamiento médico con misoprostol es una alternativa segura, efectiva y bien tolerada para las pacientes.
- Published
- 2011
40. Therapeutic Efficacy of Stable Analogues of Vasoactive Intestinal Peptide against Pathogens
- Author
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Campos-Salinas, Jenny, Cavazzuti, A., O'Valle, Francisco, Forte-Lago, Irene, Caro, Marta, Beverley, S. M., Delgado, M., González-Rey, Elena, Campos-Salinas, Jenny, Cavazzuti, A., O'Valle, Francisco, Forte-Lago, Irene, Caro, Marta, Beverley, S. M., Delgado, M., and González-Rey, Elena
- Abstract
Vasoactive intestinal peptide (VIP) is an anti-inflammatory neuropeptide recently identified as a potential antimicrobial peptide. To overcome the metabolic limitations of VIP, we modified the native peptide sequence and generated two stable synthetic analogues (VIP51 and VIP51(6–30)) with better antimicrobial profiles. Herein we investigate the effects of both VIP analogues on cell viability, membrane integrity, and ultrastructure of various bacterial strains and Leishmania species. We found that the two VIP derivatives kill various non-pathogenic and pathogenic Gram-positive and Gram-negative bacteria as well as the parasite Leishmania major through a mechanism that depends on the interaction with certain components of the microbial surface, the formation of pores, and the disruption of the surface membrane. The cytotoxicity of the VIP derivatives is specific for pathogens, because they do not affect the viability of mammalian cells. Docking simulations indicate that the chemical changes made in the analogues are critical to increase their antimicrobial activities. Consequently, we found that the native VIP is less potent as an antibacterial and fails as a leishmanicidal. Noteworthy from a therapeutic point of view is that treatment with both derivatives increases the survival and reduces bacterial load and inflammation in mice with polymicrobial sepsis. Moreover, treatment with VIP51(6–30) is very effective at reducing lesion size and parasite burden in a model of cutaneous leishmaniasis. These results indicate that the VIP analogues emerge as attractive alternatives for treating drug-resistant infectious diseases and provide key insights into a rational design of novel agents against these pathogens.
- Published
- 2014
41. Therapeutic Efficacy of Stable Analogues of Vasoactive Intestinal Peptide against Pathogens
- Author
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Campos-Salinas, Jenny, primary, Cavazzuti, Antonio, additional, O'Valle, Francisco, additional, Forte-Lago, Irene, additional, Caro, Marta, additional, Beverley, Stephen M., additional, Delgado, Mario, additional, and Gonzalez-Rey, Elena, additional
- Published
- 2014
- Full Text
- View/download PDF
42. Paradoxical effect of cortistatin treatment and its deficiency on experimental autoimmune encephalomyelitis
- Author
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Souza-Moreira, L., Morell, M., Delgado-Maroto, V., Pedreño, M., Martinez-Escudero, L., Caro, Marta, O'Valle, Francisco, Luque, Raúl M., Gallo, M., De Lecea, L., Castaño, Justo P., González-Rey, Elena, Souza-Moreira, L., Morell, M., Delgado-Maroto, V., Pedreño, M., Martinez-Escudero, L., Caro, Marta, O'Valle, Francisco, Luque, Raúl M., Gallo, M., De Lecea, L., Castaño, Justo P., and González-Rey, Elena
- Abstract
Cortistatin is a cyclic-neuropeptide produced by brain cortex and immune cells that shows potent anti-inflammatory activity. In this article, we investigated the effect of cortistatin in two models of experimental autoimmune encephalomyelitis (EAE) that mirror chronic and relapsing-remitting multiple sclerosis. A short-term systemic treatment with cortistatin reduced clinical severity and incidence of EAE, the appearance of inflammatory infiltrates in spinal cord, and the subsequent demyelination and axonal damage. This effect was associated with a reduction of the two deleterious components of the disease, namely, the autoimmune and inflammatory response. Cortistatin decreased the presence/activation of encephalitogenic Th1 and Th17 cells in periphery and nervous system, and downregulated various inflammatory mediators, whereas it increased the number of regulatory T cells with suppressive effects on the encephalitogenic response. Moreover, cortistatin regulated glial activity and favored an active program of neuroprotection/regeneration. We further used cortistatin-deficient mice to investigate the role of endogenous cortistatin in the control of immune responses. Surprisingly, cortistatin-deficient mice were partially resistant to EAE and other inflammatory disorders, despite showing competent inflammatory/autoreactive responses. This unexpected phenotype was associated with elevated circulating glucocorticoids and an anxiety-like behavior. Our findings provide a powerful rationale for the assessment of the efficacy of cortistatin as a novel multimodal therapeutic approach to treat multiple sclerosis and identify cortistatin as a key endogenous component of neuroimmune system. Copyright © 2013 by The American Association of Immunologists, Inc.
- Published
- 2013
43. Protective Role of the Neuropeptide Urocortin II against Experimental Sepsis and Leishmaniasis by Direct Killing of Pathogens
- Author
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Campos-Salinas, Jenny, primary, Caro, Marta, additional, Cavazzuti, Antonio, additional, Forte-Lago, Irene, additional, Beverley, Stephen M., additional, O’Valle, Francisco, additional, and Gonzalez-Rey, Elena, additional
- Published
- 2013
- Full Text
- View/download PDF
44. Glial innate immunity generated by non-aggregated alpha-synuclein in mouse: differences between wild-type and Parkinson's disease-linked mutants
- Author
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Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Universidad de Sevilla. Departamento de Citología e Histología Normal y Patológica, Caro, Marta, Pozo Pérez, David, Gonzalez-Rey, Elena, Delgado Mora, Mario, Fernández Montesinos, Rafael, Lachaud, Christian, Roodveldt, Cintia, Labrador Garrido, Adahir, Dobson, Christopher M., Waudby A., Christopher, Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Universidad de Sevilla. Departamento de Citología e Histología Normal y Patológica, Caro, Marta, Pozo Pérez, David, Gonzalez-Rey, Elena, Delgado Mora, Mario, Fernández Montesinos, Rafael, Lachaud, Christian, Roodveldt, Cintia, Labrador Garrido, Adahir, Dobson, Christopher M., and Waudby A., Christopher
- Published
- 2010
45. Paradoxical Effect of Cortistatin Treatment and Its Deficiency on Experimental Autoimmune Encephalomyelitis
- Author
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Souza-Moreira, Luciana, primary, Morell, Maria, additional, Delgado-Maroto, Virginia, additional, Pedreño, Marta, additional, Martinez-Escudero, Laura, additional, Caro, Marta, additional, O’Valle, Francisco, additional, Luque, Raul, additional, Gallo, Milagros, additional, de Lecea, Luis, additional, Castaño, Justo P., additional, and Gonzalez-Rey, Elena, additional
- Published
- 2013
- Full Text
- View/download PDF
46. Adipose-derived mesenchymal stromal cells induce immunomodulatory macrophages which protect from experimental colitis and sepsis
- Author
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Anderson, Per, primary, Souza-Moreira, Luciana, additional, Morell, Maria, additional, Caro, Marta, additional, O'Valle, Francisco, additional, Gonzalez-Rey, Elena, additional, and Delgado, Mario, additional
- Published
- 2012
- Full Text
- View/download PDF
47. Neuropeptides as Pleiotropic Modulators of the Immune Response
- Author
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Souza-Moreira, Luciana, primary, Campos-Salinas, Jenny, additional, Caro, Marta, additional, and Gonzalez-Rey, Elena, additional
- Published
- 2011
- Full Text
- View/download PDF
48. Glial Innate Immunity Generated by Non-Aggregated Alpha-Synuclein in Mouse: Differences between Wild-type and Parkinson's Disease-Linked Mutants
- Author
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Roodveldt, Cintia, primary, Labrador-Garrido, Adahir, additional, Gonzalez-Rey, Elena, additional, Fernandez-Montesinos, Rafael, additional, Caro, Marta, additional, Lachaud, Christian C., additional, Waudby, Christopher A., additional, Delgado, Mario, additional, Dobson, Christopher M., additional, and Pozo, David, additional
- Published
- 2010
- Full Text
- View/download PDF
49. Human amnion favours tissue repair by inducing the M1-to-M2 switch and enhancing M2 macrophage features.
- Author
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Magatti M, Vertua E, De Munari S, Caro M, Caruso M, Silini A, Delgado M, and Parolini O
- Subjects
- Animals, Cell Differentiation drug effects, Cell Proliferation drug effects, Culture Media, Conditioned pharmacology, Humans, Interleukin-6 pharmacology, Macrophages drug effects, Macrophages metabolism, Mice, Inbred C57BL, Monocytes cytology, Monocytes drug effects, Monocytes metabolism, Phagocytosis drug effects, Phenotype, Prostaglandins pharmacology, Regeneration, T-Lymphocytes cytology, T-Lymphocytes drug effects, U937 Cells, Wound Healing drug effects, Amnion physiology, Cell Polarity drug effects, Macrophages cytology
- Abstract
Human amniotic mesenchymal cells (hAMTCs) possess interesting immunomodulatory properties, making them attractive candidates for regenerative medicine applications. Recent in vivo reports argue in favour of an important role for macrophages as targets of hAMTC-mediated suppression of inflammation and the enhancement of tissue repair. However, a comprehensive study of the effects of hAMTCs and their conditioned medium (CM) on human macrophage differentiation and function is unavailable. In the present study we found that hAMTCs and CM induce the differentiation of myeloid cells (U937 and monocytes) towards macrophages. We then investigated their effects on monocytes differentiated toward pro-inflammatory M1 and anti-inflammatory M2 macrophages. Monocytes treated under M1 conditions in the presence of hAMTCs or CMs shifted towards M2-like macrophages, which expressed CD14, CD209, CD23, CD163 and PM-2 K, possessed higher phagocytic activity and produced higher IL-10 and lower pro-inflammatory cytokines. They were also poor T cell stimulators and Th1 inducers, while they were able to increase activated and naïve suppressive Treg subsets. We show that prostaglandins, and not IL-6, play a role in determining the M2 activation status. Instead, monocytes treated under M2 conditions in the presence of hAMTCs or CM retained M2-like features, but with an enhanced anti-inflammatory profile, having a reduced expression of the co-stimulatory molecule CD80, reduced phagocytosis activity and decreased the secretion of inflammatory chemokines. Importantly, we provide evidence that macrophages re-educated by CM improve tissue regeneration/repair in wound-healing models. In conclusion, we identified new cell targets of hAMTCs and their bioactive factors and here provide insight into the beneficial effects observed when these cells are used in therapeutic approaches in vivo. © 2016 The Authors Journal of Tissue Engineering and Regenerative Medicine Published by John Wiley & Sons Ltd., (© 2016 The Authors Journal of Tissue Engineering and Regenerative Medicine Published by John Wiley & Sons Ltd.)
- Published
- 2017
- Full Text
- View/download PDF
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