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dc.creatorPurroy, A. (A.)-
dc.creatorRoncal, C. (Carmen)-
dc.creatorOrbe, J. (Josune)-
dc.creatorMeilhac, O. (Olivier)-
dc.creatorBelzunce, M. (Miriam)-
dc.creatorZalba, G. (Guillermo)-
dc.creatorVilla-Bellosta, R. (Ricardo)-
dc.creatorAndres, V. (Vicente)-
dc.creatorParks, W.C. (William C.)-
dc.creatorParamo, J.A. (José Antonio)-
dc.creatorRodriguez, J.A. (José Antonio)-
dc.date.accessioned2024-02-09T11:19:18Z-
dc.date.available2024-02-09T11:19:18Z-
dc.date.issued2018-
dc.identifier.citationPurroy, A. (A.); Roncal, C. (Carmen); Orbe, J. (Josune); et al. "Matrix metalloproteinase-10 deficiency delays atherosclerosis progression and plaque calcification". Atherosclerosis. 278, 2018, 124 - 134es
dc.identifier.issn0021-9150-
dc.identifier.urihttps://hdl.handle.net/10171/68977-
dc.description.abstractBackground and aims: Matrix metalloproteinases (MMPs) have been implicated in atherosclerosis and vascular calcification. Among them, we reported that MMP10 is present in human atheroma, associated with atherosclerosis. However, it remains unclear whether MMP10 is involved in atherogenesis and vascular calcification. Methods: MMP10 was measured in serum from patients with subclinical atherosclerosis and analyzed in carotid endarterectomies by immunostaining. ApoE-deficient mice (Apoe-/-) were crossed to MMP10-deficient (Mmp10-/-) mice and followed up to 20 months. Plaque area and composition were assessed by histology and immunohistochemistry. Inflammatory markers were measured in atherosclerotic plaques by RT-qPCR, and leukocyte subpopulations were analyzed by flow cytometry. In vitro calcification assays were performed in aortic vascular smooth muscle cells (VSMC). Results: MMP10 serum levels were associated with coronary calcification in subjects with subclinical atherosclerosis. Immunostaining revealed MMP10 expression in human atheromas, spatially associated with calcification areas, and complicated plaques released higher amounts of MMP10 than non-diseased segments. Interestingly, vascular MMP10 expression was confined to the atherosclerotic lesion in Apoe-/- mice, and Apoe-/-Mmp10-/- showed a substantial reduction in atherosclerotic lesion size, macrophage content and plaque calcification. Reduced local and systemic inflammatory markers could be demonstrated in Apoe-/-Mmp10-/- by gene expression and flow cytometry analysis. Calcium phosphate deposition and vascular calcification markers were downregulated in VSMC from Apoe-/-Mmp10-/- mice. Conclusions: Delayed plaque progression and altered cellular composition in the absence of MMP10 suggests that MMP10 plays a role in atherosclerosis, favoring inflammation, development and complication of the plaque.es_ES
dc.description.sponsorshipFunded through the “UTE project CIMA” (University of Navarra), Ministerio de Educación y Ciencia (SAF2009-12039, SAF2016-79151-R), Ministerio de Sanidad y Consumo (PI14/01152 and PI15/01807), Sociedad Española de Cardiología, Sociedad Española de Arteriosclerosis, Red de Investigación Cardiovascular RIC (RD12/0042/0009), the gs5:Fondation pour la Recherche Médicale and the Fondation de France.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.rightsinfo:eu-repo/semantics/closedAccesses_ES
dc.subjectAtherosclerosises_ES
dc.subjectCalcificationes_ES
dc.subjectInflammationes_ES
dc.subjectMacrophagees_ES
dc.subjectMetalloproteinaseses_ES
dc.titleMatrix metalloproteinase-10 deficiency delays atherosclerosis progression and plaque calcificationes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.identifier.doi10.1016/j.atherosclerosis.2018.09.022-
dadun.citation.endingPage134es_ES
dadun.citation.publicationNameAtherosclerosises_ES
dadun.citation.startingPage124es_ES
dadun.citation.volume278es_ES

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