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33 results on '"Villacampa, Pilar"'

5. Angiocrine polyamine production regulates adiposity

Author

Monelli, Erika, Villacampa, Pilar, Zabala-Letona, Amaia, Martinez-Romero, Anabel, Llena, Judith, Beiroa, Daniel, Gouveia, Leonor, Chivite, Iñigo, Zagmutt, Sebastián, Gama-Perez, Pau, Osorio-Conles, Oscar, Muixi, Laia, Martinez-Gonzalez, Ainara, Castillo, Sandra D., Martín-Martín, Natalia, Castel, Pau, Valcarcel-Jimenez, Lorea, Garcia-Gonzalez, Irene, Villena, Josep A., Fernandez-Ruiz, Sonia, Serra, Dolors, Herrero, Laura, Benedito, Rui, Garcia-Roves, Pablo, Vidal, Josep, Cohen, Paul, Nogueiras, Rubén, Claret, Marc, Carracedo, Arkaitz, and Graupera, Mariona

Published
2022
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7. Endothelial TDP-43 controls sprouting angiogenesis and vascular barrier integrity, and its deletion triggers neuroinflammation

Author

Arribas, Víctor, primary, Onetti, Yara, additional, Ramiro-Pareta, Marina, additional, Villacampa, Pilar, additional, Beck, Heike, additional, Alberola, Mariona, additional, Esteve-Codina, Anna, additional, Merkel, Angelika, additional, Sperandio, Markus, additional, Martínez-Estrada, Ofelia M., additional, Schmid, Bettina, additional, and Montanez, Eloi, additional

Published
2024
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9. Chronic Glaucoma Induced in Rats by a Single Injection of Fibronectin-Loaded PLGA Microspheres: IOP-Dependent and IOP-Independent Neurodegeneration

Author

Munuera, Ines, primary, Aragon-Navas, Alba, additional, Villacampa, Pilar, additional, Gonzalez-Cela, Miriam A., additional, Subías, Manuel, additional, Pablo, Luis E., additional, Garcia-Feijoo, Julian, additional, Herrero-Vanrell, Rocio, additional, Garcia-Martin, Elena, additional, Bravo-Osuna, Irene, additional, and Rodrigo, Maria J., additional

Published
2023
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10. PI3K-C2β limits mTORC1 signaling and angiogenic growth

Author

Kobialka, Piotr, primary, Llena, Judith, additional, Deleyto-Seldas, Nerea, additional, Munar-Gelabert, Margalida, additional, Dengra, Jose A., additional, Villacampa, Pilar, additional, Albinyà-Pedrós, Alba, additional, Muixi, Laia, additional, Andrade, Jorge, additional, van Splunder, Hielke, additional, Angulo-Urarte, Ana, additional, Potente, Michael, additional, Grego-Bessa, Joaquim, additional, Castillo, Sandra D., additional, Vanhaesebroeck, Bart, additional, Efeyan, Alejo, additional, and Graupera, Mariona, additional

Published
2023
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12. Chronic Glaucoma Induced in Rats by a Single Injection of Fibronectin-Loaded PLGA Microspheres: IOP-Dependent and IOP-Independent Neurodegeneration.

Author

Munuera, Ines, Aragon-Navas, Alba, Villacampa, Pilar, Gonzalez-Cela, Miriam A., Subías, Manuel, Pablo, Luis E., Garcia-Feijoo, Julian, Herrero-Vanrell, Rocio, Garcia-Martin, Elena, Bravo-Osuna, Irene, and Rodrigo, Maria J.

Subjects
FIBRONECTINS, OPTICAL coherence tomography, MICROSPHERES, INTRAOCULAR pressure, INJECTIONS, GLAUCOMA
Abstract

To evaluate a new animal model of chronic glaucoma induced using a single injection of fibronectin-loaded biodegradable PLGA microspheres (Ms) to test prolonged therapies. 30 rats received a single injection of fibronectin-PLGA-Ms suspension (MsF) in the right eye, 10 received non-loaded PLGA-Ms suspension (Control), and 17 were non-injected (Healthy). Follow-up was performed (24 weeks), evaluating intraocular pressure (IOP), optical coherence tomography (OCT), histology and electroretinography. The right eyes underwent a progressive increase in IOP, but only induced cohorts reached hypertensive values. The three cohorts presented a progressive decrease in ganglion cell layer (GCL) thickness, corroborating physiological age-related loss of ganglion cells. Injected cohorts (MsF > Control) presented greater final GCL thickness. Histological exams explain this paradox: the MsF cohort showed lower ganglion cell counts but higher astrogliosis and immune response. A sequential trend of functional damage was recorded using scotopic electroretinography (MsF > Control > Healthy). It seems to be a function–structure correlation: in significant astrogliosis, early functional damage can be detected by electroretinography, and structural damage can be detected by histological exams but not by OCT. Males presented higher IOP and retinal and GCL thicknesses and lower electroretinography. A minimally invasive chronic glaucoma model was induced by a single injection of biodegradable Ms. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Erythema Gyratum Repens and Thyroid Cancer: a Case Report

Author

García-Malinis, Ana Julia, primary, Valverde, María Eugenia López, additional, Queipo, Francisco, additional, Puertolas-Villacampa, Pilar, additional, Linares, Dolores Planas, additional, Gilaberte, Yolanda, additional, and Agón-Banzo, Pedro Jesus, additional

Published
2022
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16. Intravitreal administration of recombinant human opticin protects against hyperoxia-induced pre-retinal neovascularization

Author

Klaska, Izabela P., primary, White, Anne, additional, Villacampa, Pilar, additional, Hoke, Justin, additional, Hervás, Laura A., additional, Maswood, Ryea N., additional, Ali, Robin R., additional, Bunce, Catey, additional, Unwin, Richard D., additional, Cooper, Garth J.S., additional, Bishop, Paul N., additional, and Bainbridge, James W., additional

Published
2021
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19. Whole body correction of mucopolysaccharidosis IIIA by intracerebrospinal fluid gene therapy

Author

Haurigot, Virginia, Marco, Sara, Ribera, Albert, Garcia, Miguel, Ruzo, Albert, Villacampa, Pilar, Ayuso, Eduard, Anor, Sonia, Andaluz, Anna, Pineda, Mercedes, Garcia-Fructuoso, Gemma, Molas, Maria, Maggioni, Luca, Munoz, Sergio, Motas, Sandra, Ruberte, Jesus, Mingozzi, Federico, Pumarola, Marti, and Bosch, Fatima

Subjects
Mucopolysaccharidosis -- Genetic aspects -- Care and treatment, Gene therapy -- Methods, Transduction -- Research, Cerebrospinal fluid -- Health aspects, Health care industry
Abstract

For most lysosomal storage diseases (LSDs) affecting the CNS, there is currently no cure. The BBB, which limits the bioavailability of drugs administered systemically, and the short half-life of lysosomal [...]

Published
2013
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20. Phosphoinositide 3-Kinase–Regulated Pericyte Maturation Governs Vascular Remodeling

Author

Figueiredo, Ana M., primary, Villacampa, Pilar, additional, Diéguez-Hurtado, Rodrigo, additional, José Lozano, Juan, additional, Kobialka, Piotr, additional, Cortazar, Ana Rosa, additional, Martinez-Romero, Anabel, additional, Angulo-Urarte, Ana, additional, Franco, Claudio A., additional, Claret, Marc, additional, Aransay, Ana María, additional, Adams, Ralf H., additional, Carracedo, Arkaitz, additional, and Graupera, Mariona, additional

Published
2020
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21. Stabilization of myeloid-derived HIFs promotes vascular regeneration in retinal ischemia

Author

Villacampa, Pilar, primary, Liyanage, Sidath E., additional, Klaska, Izabela P., additional, Cristante, Enrico, additional, Menger, Katja E., additional, Sampson, Robert D., additional, Barlow, Maeve, additional, Abelleira-Hervas, Laura, additional, Duran, Yanai, additional, Smith, Alexander J., additional, Ali, Robin R., additional, Luhmann, Ulrich F. O., additional, and Bainbridge, James W. B., additional

Published
2019
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22. Myeloid-Derived Vascular Endothelial Growth Factor and Hypoxia-Inducible Factor Are Dispensable for Ocular Neovascularization—Brief Report

Author

Liyanage, Sidath E., Fantin, Alessandro, Villacampa, Pilar, Lange, Clemens A., Denti, Laura, Cristante, Enrico, Smith, Alexander J., Ali, Robin R., Luhmann, Ulrich F., Bainbridge, James W., and Ruhrberg, Christiana

Subjects
Mice, Knockout, Vascular Endothelial Growth Factor A, macular degeneration, Basic Sciences, Retinal Vessels, Retinal Neovascularization, Hypoxia-Inducible Factor 1, alpha Subunit, choroidal neovascularization, Oxygen, diabetic retinopathy, Disease Models, Animal, Animals, Newborn, myeloid cells, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, Basic Helix-Loop-Helix Transcription Factors, Animals, Retinopathy of Prematurity, Signal Transduction
Abstract

Supplemental Digital Content is available in the text., Objective— Ocular neovascularization (ONV) is a pathological feature of sight-threatening human diseases, such as diabetic retinopathy and age-related macular degeneration. Macrophage depletion in mouse models of ONV reduces the formation of pathological blood vessels, and myeloid cells are widely considered an important source of the vascular endothelial growth factor A (VEGF). However, the importance of VEGF or its upstream regulators hypoxia-inducible factor-1α (HIF1α) and hypoxia-inducible factor-2α (HIF2α) as myeloid-derived regulators of ONV remains to be determined. Approach and Results— We used 2 mouse models of ONV, choroidal neovascularization and oxygen-induced retinopathy, to show that Vegfa is highly expressed by several cell types, but not myeloid cells during ONV. Moreover, myeloid-specific VEGF ablation did not reduce total ocular VEGF during choroidal neovascularization or oxygen-induced retinopathy. In agreement, the conditional inactivation of Vegfa, Hif1a, or Epas1 in recruited and resident myeloid cells that accumulated at sites of neovascularization did not significantly reduce choroidal neovascularization or oxygen-induced retinopathy. Conclusions— The finding that myeloid cells are not a significant local source of VEGF in these rodent models of ONV suggests that myeloid function in neovascular eye disease differs from skin wound healing and other neovascular pathologies.

Published
2015

24. Disease correction by AAV-mediated gene therapy in a new mouse model of mucopolysaccharidosis type IIID

Author

Roca, Carles, primary, Motas, Sandra, additional, Marcó, Sara, additional, Ribera, Albert, additional, Sánchez, Víctor, additional, Sánchez, Xavier, additional, Bertolin, Joan, additional, León, Xavier, additional, Pérez, Jennifer, additional, Garcia, Miguel, additional, Villacampa, Pilar, additional, Ruberte, Jesús, additional, Pujol, Anna, additional, Haurigot, Virginia, additional, and Bosch, Fatima, additional

Published
2017
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25. Progressive neurologic and somatic disease in a novel model of human Mucopolysaccharidosis type IIIC

Author

Marcó, Sara, primary, Pujol, Anna, additional, Roca, Carles, additional, Motas, Sandra, additional, Ribera, Albert, additional, Garcia, Miguel, additional, Molas, Maria, additional, Villacampa, Pilar, additional, Melia, Cristian S., additional, Sánchez, Víctor, additional, Sánchez, Xavier, additional, Bertolin, Joan, additional, Ruberte, Jesús, additional, Haurigot, Virginia, additional, and Bosch, Fatima, additional

Published
2016
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26. Myeloid-Derived Vascular Endothelial Growth Factor and Hypoxia-Inducible Factor Are Dispensable for Ocular Neovascularization—Brief Report

Author

Liyanage, Sidath E., primary, Fantin, Alessandro, additional, Villacampa, Pilar, additional, Lange, Clemens A., additional, Denti, Laura, additional, Cristante, Enrico, additional, Smith, Alexander J., additional, Ali, Robin R., additional, Luhmann, Ulrich F., additional, Bainbridge, James W., additional, and Ruhrberg, Christiana, additional

Published
2016
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28. Biochemical, histological and functional correction of mucopolysaccharidosis Type IIIB by intra-cerebrospinal fluid gene therapy

Author

Ribera, Albert, primary, Haurigot, Virginia, additional, Garcia, Miguel, additional, Marcó, Sara, additional, Motas, Sandra, additional, Villacampa, Pilar, additional, Maggioni, Luca, additional, León, Xavier, additional, Molas, Maria, additional, Sánchez, Víctor, additional, Muñoz, Sergio, additional, Leborgne, Christian, additional, Moll, Xavier, additional, Pumarola, Martí, additional, Mingozzi, Federico, additional, Ruberte, Jesús, additional, Añor, Sònia, additional, and Bosch, Fatima, additional

Published
2014
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29. Correction of Pathological Accumulation of Glycosaminoglycans in Central Nervous System and Peripheral Tissues of MPSIIIA Mice Through Systemic AAV9 Gene Transfer

Author

Ruzo, Albert, primary, Marcó, Sara, additional, García, Miquel, additional, Villacampa, Pilar, additional, Ribera, Albert, additional, Ayuso, Eduard, additional, Maggioni, Lucca, additional, Mingozzi, Federico, additional, Haurigot, Virginia, additional, and Bosch, Fatima, additional

Published
2012
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32. Progressive neurologic and somatic disease in a novel mouse model of human mucopolysaccharidosis type IIIC

Author

Marcó, Sara, Pujol, Anna, Roca, Carles, Motas, Sandra, Ribera, Albert, Garcia, Miguel, Molas, Maria, Villacampa, Pilar, Melia, Cristian S., Sánchez, Víctor, Sánchez, Xavier, Bertolin, Joan, Ruberte, Jesús, Haurigot, Virginia, and Bosch, Fatima

Abstract

Mucopolysaccharidosis type IIIC (MPSIIIC) is a severe lysosomal storage disease caused by deficiency in activity of the transmembrane enzyme heparan-α-glucosaminide N-acetyltransferase (HGSNAT) that catalyses the N-acetylation of α-glucosamine residues of heparan sulfate. Enzyme deficiency causes abnormal substrate accumulation in lysosomes, leading to progressive and severe neurodegeneration, somatic pathology and early death. There is no cure for MPSIIIC, and development of new therapies is challenging because of the unfeasibility of cross-correction. In this study, we generated a new mouse model of MPSIIIC by targeted disruption of the Hgsnat gene. Successful targeting left LacZ expression under control of the Hgsnat promoter, allowing investigation into sites of endogenous expression, which was particularly prominent in the CNS, but was also detectable in peripheral organs. Signs of CNS storage pathology, including glycosaminoglycan accumulation, lysosomal distension, lysosomal dysfunction and neuroinflammation were detected in 2-month-old animals and progressed with age. Glycosaminoglycan accumulation and ultrastructural changes were also observed in most somatic organs, but lysosomal pathology seemed most severe in liver. Furthermore, HGSNAT-deficient mice had altered locomotor and exploratory activity and shortened lifespan. Hence, this animal model recapitulates human MPSIIIC and provides a useful tool for the study of disease physiopathology and the development of new therapeutic approaches.

Published
2016
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33. Increased Intraocular IGF-I Induces Blood-Retinal Barrier Breakdown in a Transgenic Animal Model of Diabetic Retinopathy.

Author

Haurigot, Virginia, Villacampa, Pilar, Bosch, Assumpció, Llombart, Cristina, Ribera, Albert, Ruberte, Jesus, and Bosch, Fatima

Subjects
*GROWTH factors, *DIABETIC retinopathy, *TRANSGENIC mice, *RETINA, *FLUORESCENCE, *ELECTRON microscopy
Abstract

Blood-retinal barrier (BRB) breakdown is an important feature of non-proliferative diabetic retinopathy and other diverse ocular disorders. The leakage of plasma components through a disrupted barrier can alter the extracellular milieu, affect retinal neuronal function and eventually lead to macular edema, a major cause of visual loss. Several growth factors, such as Insulin Growth Factor-I (IGF-I) are believed to be involved in pathological vascular permeability. However, the source of increased intraocular IGF-I in diabetic retinopathy is controversial and the relative contributions of local or serum IGF-I is unknown. Here, we investigated BRB breakdown in normoglycemic/normoinsulinemic transgenic mice overexpressing IGF-I in the retina. IGF-I induced a progressive increase in vascular leakage beginning at 3 month of age. Transgenic vessels were permeable to both low molecular weight compounds and proteins. In vivo fluorescence imaging confirmed extravasation of solutes in transgenic eyes. Electron microscopy analyses of HRP-injected transgenic retinas revealed increased transcytosis and increased paracellular flux through disrupted endothelial tight junctions. The latter was accompanied by altered expression of the tight junction complex proteins. To assess the contribution of circulating IGF-I to BRB breakdown we studied another transgenic animal model expressing growth hormone in the liver. These mice had increased serum but normal intraocular IGF-I levels. Transgenic animals had morphologically normal eyes and BRB breakdown was not detectable even with the most sensitive techniques. Furthermore, long term diabetes did not favour the appearance of a leaky phenotype in these animals. In conclusion, this study provides evidence for a key role of increased intraocular IGF-I in the breakdown of blood-retinal barrier. [ABSTRACT FROM AUTHOR]

Published
2007

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