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. 2019 Nov 1;33(21-22):1491–1505. doi: 10.1101/gad.329763.119

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© 2019 Xiao et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — Lats1/2 deletion in uninjured cardiac fibroblasts results in pervasive myocardial fibrosis. (A) Experimental strategy for cardiac fibroblast Cre activation and tissue collection. (B) Survival curve of control mice (Tcf21^iCre/+; Rosa26^mTmG/+) and Lats1/2 CKO (Tcf21^iCre/+; Lats1/2^flox/flox; Rosa26^mTmG/+) mice by 3 wk after Cre activation and sham. (C) Representative gross heart morphology at 3 wk after Cre activation. Atria were stiffened and enlarged (asterisks). Scale bar, 200 µm. (D) Representative Masson's trichrome serial sections of control and Lats1/2 CKO hearts. Lats1/2 CKO hearts possessed expansive and aggregated (arrows) cardiac fibrosis (stained blue) within the myocardium (stained red). Scale bar, 1000 µm. (E) Representative M-mode and B-mode echocardiographic images of control and Lats1/2 CKO mouse hearts 3 wk after tamoxifen induction. (F) Percent ejection fraction, fractional shortening, and cardiac output as determined by echocardiography. Control, n = 10; Lats1/2 CKO, n = 7. Statistical significance was determined by t-test, P-value <0.05.