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http://hdl.handle.net/2445/194621
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DC Field | Value | Language |
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dc.contributor.author | Alonso-Herranz, Laura | - |
dc.contributor.author | Sahún-Español, Álvaro | - |
dc.contributor.author | Paredes, Ana | - |
dc.contributor.author | Gonzalo, Pilar | - |
dc.contributor.author | Gkontra, Polyxeni | - |
dc.contributor.author | Núñez, Vanessa | - |
dc.contributor.author | Clemente, Cristina | - |
dc.contributor.author | Cedenilla, Marta | - |
dc.contributor.author | Villalba-Orero, María | - |
dc.contributor.author | Inserte, Javier | - |
dc.contributor.author | García-Dorado, David | - |
dc.contributor.author | García Arroyo, Alicia | - |
dc.contributor.author | Ricote, Mercedes | - |
dc.date.accessioned | 2023-03-03T17:55:32Z | - |
dc.date.available | 2023-03-03T17:55:32Z | - |
dc.date.issued | 2020-10-16 | - |
dc.identifier.issn | 2050-084X | - |
dc.identifier.uri | http://hdl.handle.net/2445/194621 | - |
dc.description.abstract | Macrophages (M $\varphi s$ ) produce factors that participate in cardiac repair and remodeling after myocardial infarction (MI); however, how these factors crosstalk with other cell types mediating repair is not fully understood. Here we demonstrated that cardiac M $\varphi$ s increased the expression of Mmp14 (MT1-MMP) 7 days post-MI. We selectively inactivated the $M m p 14$ gene in $\mathrm{M} \varphi$ s using a genetic strategy (Mmp14ff: Lyz2-Cre). This conditional KO (MAC-Mmp14 KO) resulted in attenuated post-MI cardiac dysfunction, reduced fibrosis, and preserved cardiac capillary network. Mechanistically, we showed that MT1-MMP activates latent TGF $\beta 1$ in M $\varphi$ s, leading to paracrine SMAD2-mediated signaling in endothelial cells (ECs) and endothelial-to-mesenchymal transition (EndMT). Post-MI MAC-Mmp14 KO hearts contained fewer cells undergoing EndMT than their wild-type counterparts, and Mmp14-deficient $\mathrm{M} \varphi \mathrm{s}$ showed a reduced ability to induce EndMT in co-cultures with ECs. Our results indicate the contribution of EndMT to cardiac fibrosis and adverse remodeling post-MI and identify M $\varphi$ MT1-MMP as a key regulator of this process. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | eLife Sciences | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.7554/eLife.57920 | - |
dc.relation.ispartof | eLife, 2020 | - |
dc.relation.uri | https://doi.org/10.7554/eLife.57920 | - |
dc.rights | cc-by (c) Alonso-Herranz, Laura et al., 2020 | - |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | - |
dc.source | Articles publicats en revistes (Matemàtiques i Informàtica) | - |
dc.subject.classification | Infart de miocardi | - |
dc.subject.classification | Codi genètic | - |
dc.subject.classification | Cultiu cel·lular | - |
dc.subject.classification | Malalties cardiovasculars | - |
dc.subject.other | Myocardial infarction | - |
dc.subject.other | Genetic code | - |
dc.subject.other | Cell culture | - |
dc.subject.other | Cardiovascular diseases | - |
dc.title | Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/ TGF$\beta 1$ after myocardial infarction | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 731727 | - |
dc.date.updated | 2023-03-03T17:55:32Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
Appears in Collections: | Articles publicats en revistes (Matemàtiques i Informàtica) |
Files in This Item:
File | Description | Size | Format | |
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731727.pdf | 7.08 MB | Adobe PDF | View/Open |
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