Assessing the effect of myofibroblast depletion for Yap and Wwtr1 by single Cell RNAsequencing within ventricular interstitial cells 6 days post surgical MI.

To assess the pathophysiological of genetic depletion of Yap and Wwtr1 in myofibroblasts following myocardial infarction, we utilized a Cre-lox system whereby the inducible Periostin promoter is leveraged to deplete both Yap and Wwtr1 from myofibroblasts in mice. Following myocardial infarction, myofibroblast depletion of both Yap and Wwtr1 significantly improves cardiac function after injury as compared to injured controls. Here, we have performed single cell RNA sequencing of interstitial cardiac cells 7 days post myocardial infarction to assess differentially express genes within cardiac fibroblasts and immune cell populations. Overall design: After surgically ligating the left anterior descending artery, mice were adminstered tamoxifen containing chow to excise Yap and a singel copy of Wwtr1 from Periostin expressing myofibroblasts (Yapfl/fl;Wwtr1fl/+;PostnMCM) or control for Cre toxicity (PostnMCM). Both strains carried the R26-eGFP transgene.