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- W3093178500 abstract "Macrophages (Mφs) 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 Mφs increased the expression of Mmp14 (MT1-MMP) 7 days post-MI. We selectively inactivated the Mmp14 gene in Mφs using a genetic strategy ( Mmp14 f/f : 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 TGFβ1 in Mφs, 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 Mφs 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 Mφ MT1-MMP as a key regulator of this process." @default.
- W3093178500 created "2020-10-22" @default.
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- W3093178500 date "2020-10-16" @default.
- W3093178500 modified "2023-10-08" @default.
- W3093178500 title "Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/TGFβ1 after myocardial infarction" @default.
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- W3093178500 doi "https://doi.org/10.7554/elife.57920" @default.
- W3093178500 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7609061" @default.
- W3093178500 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33063665" @default.
- W3093178500 hasPublicationYear "2020" @default.
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