14 results on '"Vallin, Benjamin"'
Search Results
2. Dual inhibitory mechanism of the truncated form of adenylyl cyclase 8 in cell signal integration: Structural and functional approaches
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Legueux-Cajgfinger, Yohan, primary, Velusamy, Mahesh, additional, Fathallah, Samar, additional, Vallin, Benjamin, additional, Duca, Laurent, additional, Dauchez, Manuel, additional, Vincent, Pierre, additional, Limon, Isabelle, additional, and Blaise, Régis, additional
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- 2023
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3. Selective neurodegeneration generated by intravenous α‐synuclein pre‐formed fibril administration is not associated with endogenous α‐synuclein levels in the rat brain
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Kuan, Wei‐Li, primary, Alfaidi, Maha, additional, Horne, Catherine B., additional, Vallin, Benjamin, additional, Fox, Sarah, additional, Fazal, Shaline V., additional, Williams‐Gray, Caroline H., additional, and Barker, Roger A., additional
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- 2022
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4. Selective neurodegeneration generated by intravenous α-synuclein pre-formed fibril administration is not associated with endogenous α-synuclein levels in the rat brain
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Kuan, Wei-Li, Alfaidi, Maha, Horne, Catherine B, Vallin, Benjamin, Fox, Sarah, Fazal, Shaline V, Williams-Gray, Caroline H, Barker, Roger A, Kuan, Wei-Li [0000-0002-0273-1320], and Apollo - University of Cambridge Repository
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α-synuclein ,rabies virus glycoprotein (RVG) ,Dopaminergic Neurons ,neurodegeneration ,selective vulnerability ,alpha-Synuclein ,Animals ,Brain ,Parkinson Disease ,Administration, Intravenous ,pre-formed fibrils ,Rats - Abstract
Selective loss of discrete neuronal populations is a prominent feature of many neurodegenerative conditions, but the molecular basis of this is poorly understood. A central role of α-synuclein in the selective neurodegeneration of Parkinson's disease has been speculated, as its level of expression critically determines the propensity of this protein to misfold. To investigate whether the propensity of neuronal cell loss is associated with the level of endogenous α-synuclein expression, non-transgenic rats were given a single intravenous administration of α-synuclein pre-formed fibrils (PFFs) reversibly complexed with the rabies virus glycoprotein peptide (RVG9R). The number of surviving cells in different neuronal populations was systematically quantified using unbiased stereology. Our data demonstrated that a non-selective, transvascular delivery of α-synuclein PFFs led to a time-dependent loss of specific populations of midbrain (but not olfactory) dopaminergic neurons, medullary (but not pontine) cholinergic neurons, and brainstem serotonergic neurons. Contrary to the central role of endogenous α-synuclein expression in determining the seeding and aggregation propensity of pathological α-synuclein, we did not observe an association between the levels of α-synuclein expression in different regions of the rodent brain (although did not ascertain this at the individual cell level) and neurodegenerative propensity. The results from our study highlight the complexity of the neurodegenerative process generated by α-synuclein seeding. Further investigations are therefore required to elucidate the molecular basis of neurodegeneration driven by exogenous pathogenic α-synuclein spread.
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- 2022
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- View/download PDF
5. Selective neurodegeneration generated by intravenous α‐synuclein pre‐formed fibril administration is not associated with endogenous α‐synuclein levels in the rat brain.
- Author
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Kuan, Wei‐Li, Alfaidi, Maha, Horne, Catherine B., Vallin, Benjamin, Fox, Sarah, Fazal, Shaline V., Williams‐Gray, Caroline H., and Barker, Roger A.
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ALPHA-synuclein ,RAPHE nuclei ,DOPAMINERGIC neurons ,PEPTIDES ,PARKINSON'S disease ,NEURODEGENERATION ,RABIES virus - Abstract
Selective loss of discrete neuronal populations is a prominent feature of many neurodegenerative conditions, but the molecular basis of this is poorly understood. A central role of α‐synuclein in the selective neurodegeneration of Parkinson's disease has been speculated, as its level of expression critically determines the propensity of this protein to misfold. To investigate whether the propensity of neuronal cell loss is associated with the level of endogenous α‐synuclein expression, non‐transgenic rats were given a single intravenous administration of α‐synuclein pre‐formed fibrils (PFFs) reversibly complexed with the rabies virus glycoprotein peptide (RVG9R). The number of surviving cells in different neuronal populations was systematically quantified using unbiased stereology. Our data demonstrated that a non‐selective, transvascular delivery of α‐synuclein PFFs led to a time‐dependent loss of specific populations of midbrain (but not olfactory) dopaminergic neurons, medullary (but not pontine) cholinergic neurons, and brainstem serotonergic neurons. Contrary to the central role of endogenous α‐synuclein expression in determining the seeding and aggregation propensity of pathological α‐synuclein, we did not observe an association between the levels of α‐synuclein expression in different regions of the rodent brain (although did not ascertain this at the individual cell level) and neurodegenerative propensity. The results from our study highlight the complexity of the neurodegenerative process generated by α‐synuclein seeding. Further investigations are therefore required to elucidate the molecular basis of neurodegeneration driven by exogenous pathogenic α‐synuclein spread. [ABSTRACT FROM AUTHOR]
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- 2023
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- View/download PDF
6. Reduced expression of dopamine D2 receptors on astrocytes in R6/1 HD mice and HD post-mortem tissue
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Harris, Kate L., primary, Mason, Sarah L., additional, Vallin, Benjamin, additional, and Barker, Roger A., additional
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- 2022
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7. Identification of a new adenylyl cyclase 8 isoform - implication in vascular smooth muscle cells trans-differentiation and pathological vascular remodeling: PO.037
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Vallin, Benjamin, Clément, Nathalie, Blaise, Régis, and Limon, Isabelle
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- 2016
8. Slug, a Cancer‐Related Transcription Factor, is Involved in Vascular Smooth Muscle Cell Transdifferentiation Induced by Platelet‐Derived Growth Factor‐BB During Atherosclerosis
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Ledard, Nahema, Liboz, Alexandrine, Blondeau, Bertrand, Babiak, Mégane, Moulin, Célia, Vallin, Benjamin, Guillas, Isabelle, Mateo, Véronique, Jumeau, Claire, Blirando, Karl, Meilhac, Olivier, Limon, Isabelle, Glorian, Martine, Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Sorbonne Université (SU), Centre de Recherche Saint-Antoine (CR Saint-Antoine), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Institute of cardiometabolism and nutrition (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU), Centre d'Immunologie et de Maladies Infectieuses (CIMI), Physiopathologie des maladies génétiques d'expression pédiatrique, Diabète athérothrombose et thérapies Réunion Océan Indien (DéTROI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de La Réunion (UR), Université de La Réunion (UR), Cyclotron Réunion Océan Indien (CYROI), Université de La Réunion (UR)-Centre Hospitalier Universitaire de La Réunion (CHU La Réunion), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Physiopathologie des maladies génétiques d'expression pédiatrique (UMRS_933), Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Immunologie et des Maladies Infectieuses (CIMI), and Dieu-Nosjean, Marie-Caroline
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animal structures ,[SDV]Life Sciences [q-bio] ,Myocytes, Smooth Muscle ,Becaplermin ,Dinoprostone ,Muscle, Smooth, Vascular ,[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system ,Vascular Disease ,La R eunion (O.M.) ,Animals ,Humans ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,atherogenesis inflammation vascular smooth muscle --CYROI ,Extracellular Signal-Regulated MAP Kinases ,Cells, Cultured ,Original Research ,Sainte Clotilde ,Myosin Heavy Chains ,Cardio‐Oncology Spotlight ,fungi ,atherogenesis ,Atherosclerosis ,Rats ,[SDV] Life Sciences [q-bio] ,inflammation ,vascular smooth muscle ,Cell Transdifferentiation ,embryonic structures ,Snail Family Transcription Factors ,vascular smooth muscle --CYROI ,Signal Transduction - Abstract
International audience; Background Heart attacks and stroke often result from occlusive thrombi following the rupture of vulnerable atherosclerotic plaques. Vascular smooth muscle cells (VSMCs) play a pivotal role in plaque vulnerability because of their switch towards a proinflammatory/macrophage-like phenotype when in the context of atherosclerosis. The prometastatic transcription factor Slug/Snail2 is a critical regulator of cell phenotypic transition. Here, we aimed to investigate the role of Slug in the transdifferentiation process of VSMCs occurring during atherogenesis. Methods and Results In rat and human primary aortic smooth muscle cells, Slug protein expression is strongly and rapidly increased by platelet-derived growth factor-BB (PDGF-BB). PDGF-BB increases Slug protein without affecting mRNA levels indicating that this growth factor stabilizes Slug protein. Immunocytochemistry and subcellular fractionation experiments reveal that PDGF-BB triggers a rapid accumulation of Slug in VSMC nuclei. Using pharmacological tools, we show that the PDGF-BB-dependent mechanism of Slug stabilization in VSMCs involves the extracellular signal-regulated kinase 1/2 pathway. Immunohistochemistry experiments on type V and type VI atherosclerotic lesions of human carotids show smooth muscle-specific myosin heavy chain-/Slug-positive cells surrounding the prothrombotic lipid core. In VSMCs, Slug siRNAs inhibit prostaglandin E2 secretion and prevent the inhibition of cholesterol efflux gene expression mediated by PDGF-BB, known to be involved in plaque vulnerability and/or thrombogenicity. Conclusions Our results highlight, for the first time, a role of Slug in aortic smooth muscle cell transdifferentiation and enable us to consider Slug as an actor playing a role in the atherosclerotic plaque progression towards a life-threatening phenotype. This also argues for common features between acute cardiovascular events and cancer.
- Published
- 2020
9. A fluorescent molecular imaging probe with selectivity for soluble tau aggregated protein
- Author
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Zhao, Yanyan, primary, Tietz, Ole, additional, Kuan, Wei-Li, additional, Haji-Dheere, Abdul K., additional, Thompson, Stephen, additional, Vallin, Benjamin, additional, Ronchi, Elisabetta, additional, Tóth, Gergely, additional, Klenerman, David, additional, and Aigbirhio, Franklin I., additional
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- 2020
- Full Text
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10. Cardiac adenylyl cyclase overexpression precipitates and aggravates age-related myocardial dysfunction
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Mougenot, Nathalie, primary, Mika, Delphine, additional, Czibik, Gabor, additional, Marcos, Elizabeth, additional, Abid, Shariq, additional, Houssaini, Amal, additional, Vallin, Benjamin, additional, Guellich, Aziz, additional, Mehel, Hind, additional, Sawaki, Daigo, additional, Vandecasteele, Grégoire, additional, Fischmeister, Rodolphe, additional, Hajjar, Roger J, additional, Dubois-Randé, Jean-Luc, additional, Limon, Isabelle, additional, Adnot, Serge, additional, Derumeaux, Geneviève, additional, and Lipskaia, Larissa, additional
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- 2019
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11. Caractérisation fonctionnelle de nouvelles isoformes d'adénylyl cyclase 8 identifiées dans les cellules musculaires lisses vasculaires trans-différenciées
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Vallin, Benjamin, Adaptation Biologique et Vieillissement = Biological Adaptation and Ageing (B2A), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris VI, Régis Blaise, Isabelle Limon, Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Adenylyl cyclase 8 ,Vascular smooth muscle cell ,Cyclic AMP ,[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO] ,Cellule musculaire lisse vasculaire ,Trans-différenciation ,AMP cyclique ,Dominant-négatif ,Hétéro-dimérisation ,Adénylyl cyclase 8 - Abstract
The phenotypic switch of vascular smooth muscle cells (VSMC) towards a migratory, proliferative and secretory state plays a key role in atherosclerotic plaque expansion and intimal hyperplasia leading to post-angioplasty restenosis. Our previous results suggest that the trans-differentiation of rat, mouse and human VSMC involves the de novo expression of the Adenylyl Cyclase 8 (AC8), an enzyme that catalyzes the synthesis of cyclic AMP (cAMP) (Clement et al., 2006; Gueguen et al., 2010; Keuylian et al., 2012; unpublished results). The main goal of my PhD was to decipher the impact of AC8 expression on cAMP signaling in trans-differentiated VSMC. Using the FRET-based biosensor T-Epac-VV, we showed that the de novo expression of AC8 limits increases in cellular cAMP. This non-canonical function relies on a new family of AC8 isoforms that we have identified and cloned: the AC8E1 to 4. They share a common deletion of the first five transmembrane domains. The biochemical characterization of AC8E over-expressed in HEK cells allowed us to elucidate their functioning. cAMP accumulation assays, co-immunoprecipitation experiments and immunocytochemistry revealed that AC8E hetero-dimerize with functional AC during their maturation in the reticulum, suppress their enzymatic activity and prevent their traffic to the plasma membrane. Numerous studies have shown that increases in cAMP concentration within trans-differentiated VSMC antagonize pathological vascular remodeling (Douglas et al., 2005; Katakami et al., 2010). Thus, the induction of AC8E in trans-differentiated VSMC could prevent the vasculoprotective effects of cAMP and promote the acquisition of a synthetic phenotype.; La trans-différenciation des cellules musculaires lisses vasculaires (CMLV) vers un phénotype migratoire, prolifératif et sécrétoire joue un rôle clé dans la progression des lésions athéromateuses et l’hyperplasie intimale qui sous-tend la resténose post-angioplastie. Nos travaux suggèrent que la transition phénotypique des CMLV implique, chez le rat, la souris et l’Homme, l’expression de novo de l’Adénylyl Cyclase 8 (AC8), une enzyme catalysant la synthèse de l’AMP cyclique (AMPc) (Clément et al., 2006; Gueguen et al., 2010; Keuylian et al., 2012; résultats non publiés). Ce travail de thèse avait pour objectif d’appréhender le rôle de l’AC8 dans la trans-différenciation des CMLV en évaluant son impact sur la signalisation AMPc. L’étude des dynamiques de production du second messager avec le biosenseur T-Epac-VV montre que l’AC8 inhibe les hausses d’AMPc dans les CMLV trans-différenciées à l’Interleukine-1β. Cette fonction non canonique est assurée par de nouvelles isoformes d’AC8 que nous avons identifiées et clonées, les AC8E1 à 4, qui partagent une délétion des cinq premiers domaines transmembranaires. Des dosages de l’accumulation d’AMPc couplés à des expériences de co-immunoprécipitation et d’immunocytochimie révèlent que les AC8E exprimées de façon hétérologue dans des cellules HEK s’hétéro-dimérisent avec les AC en transit dans le réticulum, suppriment leur activité enzymatique et préviennent leur adressage à la membrane plasmique. L’induction des AC8E dans les CMLV trans-différenciées pourrait prévenir les effets vasculoprotecteurs de l’AMPc (Douglas et al., 2005; Katakami et al., 2010), favorisant ainsi l’acquisition et/ou le maintien du phénotype synthétique.
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- 2017
12. Novel short isoforms of adenylyl cyclase as negative regulators of cAMP production
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Vallin, Benjamin, primary, Legueux-Cajgfinger, Yohan, additional, Clément, Nathalie, additional, Glorian, Martine, additional, Duca, Laurent, additional, Vincent, Pierre, additional, Limon, Isabelle, additional, and Blaise, Régis, additional
- Published
- 2018
- Full Text
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13. Adénylyl cyclases et transdifférenciation des cellules musculaires lisses vasculaires : rôle dans le remodelage vasculaire pathologique
- Author
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Gueguen, Marie, primary, Vallin, Benjamin, additional, Glorian, Martine, additional, Blaise, Régis, additional, and Limon, Isabelle, additional
- Published
- 2016
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14. Slug, a Cancer-Related Transcription Factor, is Involved in Vascular Smooth Muscle Cell Transdifferentiation Induced by Platelet-Derived Growth Factor-BB During Atherosclerosis.
- Author
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Ledard N, Liboz A, Blondeau B, Babiak M, Moulin C, Vallin B, Guillas I, Mateo V, Jumeau C, Blirando K, Meilhac O, Limon I, and Glorian M
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- Animals, Atherosclerosis genetics, Atherosclerosis pathology, Cells, Cultured, Dinoprostone metabolism, Extracellular Signal-Regulated MAP Kinases metabolism, Humans, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle metabolism, Myocytes, Smooth Muscle pathology, Myosin Heavy Chains metabolism, Rats, Signal Transduction, Snail Family Transcription Factors genetics, Atherosclerosis metabolism, Becaplermin pharmacology, Cell Transdifferentiation drug effects, Muscle, Smooth, Vascular drug effects, Myocytes, Smooth Muscle drug effects, Snail Family Transcription Factors metabolism
- Abstract
Background Heart attacks and stroke often result from occlusive thrombi following the rupture of vulnerable atherosclerotic plaques. Vascular smooth muscle cells (VSMCs) play a pivotal role in plaque vulnerability because of their switch towards a proinflammatory/macrophage-like phenotype when in the context of atherosclerosis. The prometastatic transcription factor Slug/Snail2 is a critical regulator of cell phenotypic transition. Here, we aimed to investigate the role of Slug in the transdifferentiation process of VSMCs occurring during atherogenesis. Methods and Results In rat and human primary aortic smooth muscle cells, Slug protein expression is strongly and rapidly increased by platelet-derived growth factor-BB (PDGF-BB). PDGF-BB increases Slug protein without affecting mRNA levels indicating that this growth factor stabilizes Slug protein. Immunocytochemistry and subcellular fractionation experiments reveal that PDGF-BB triggers a rapid accumulation of Slug in VSMC nuclei. Using pharmacological tools, we show that the PDGF-BB-dependent mechanism of Slug stabilization in VSMCs involves the extracellular signal-regulated kinase 1/2 pathway. Immunohistochemistry experiments on type V and type VI atherosclerotic lesions of human carotids show smooth muscle-specific myosin heavy chain-/Slug-positive cells surrounding the prothrombotic lipid core. In VSMCs, Slug siRNAs inhibit prostaglandin E2 secretion and prevent the inhibition of cholesterol efflux gene expression mediated by PDGF-BB, known to be involved in plaque vulnerability and/or thrombogenicity. Conclusions Our results highlight, for the first time, a role of Slug in aortic smooth muscle cell transdifferentiation and enable us to consider Slug as an actor playing a role in the atherosclerotic plaque progression towards a life-threatening phenotype. This also argues for common features between acute cardiovascular events and cancer.
- Published
- 2020
- Full Text
- View/download PDF
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