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. 2020 Jun 30;11:669. doi: 10.3389/fphys.2020.00669

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Copyright © 2020 Shi, Xiao, Liu, Chen, Xu, Fan and Yin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Notch3 alleviates cardiac fibrosis after myocardial infarction via the RhoA/ROCK/Hif1α pathway. (A,B) Notch3 overexpression in the myocardium after Ad-N3ICD injection was confirmed by RT-qPCR and western blot (n = 5). (C) Measurements of cardiac function indices of rats in each group 2 months after myocardial infarction (MI) injury (n = 5). (D) Masson staining of the rat heart tissues. The positively stained area (blue) represents fibrosis (n = 5). (E) Western blot analysis and quantitative results of α-SMA, RhoA, ROCK1, ROCK2, and Hif1α (n = 5). (F) Western blot analysis of membrane-bound RhoA and cadherins in rat hearts from different treatments. Values represent the mean ± SD. *P < 0.05, **P < 0.01. M-RhoA, membrane RhoA; C-RhoA, cytosolic RhoA; M-pan cadherin, membrane pan cadherin; C-pan cadherin, cytosolic pan cadherin; M-β-actin, membrane β-actin; C-β-actin, cytosolic β-actin.