Background We have shown enhanced expression of transforming growth factor (TGF)- β1 and collagen in heart in response to pressure overload stress induced by transverse aortic constriction (TAC).
Hypothesis Cardiac fibrosis/remodeling in response to TAC is blunted in dominant negative TGF-β receptor II (DnTGFβRII) mice in which the profibrogenic effect of TGF-β is blocked.
Method Adult male DnTGFβRII and wild-type nontransgenic (NTG) mice were given 25 mM ZnSO4 in their drinking water for 2 weeks prior to TAC or sham surgery in order to induce DnTGFβ type II receptor expression. One week later, echocardiogram was done to evaluate heart function and then hearts were weighed and analyzed for collagen content. Collagen volume percent in the interstitial and perivascular regions of the left ventricle (LV) was measured using picrosirius red staining.
Results and Conclusion Cardiac hypertrophy, with unchanged heart function, developed in both DnTGFβRII and NTG mice 1 week post TAC. The TAC-induced cardiac hypertrophy was accompanied by an increase in collagen volume in the interstitial space of NTG, but not DnTGFβRII mice. Interestingly, the TAC-induced perivascular collagen deposition in response to pressure overload stress was exaggerated in DnTGFβRII mice. These findings(figure) support our hypothesis that TGF-β is an important modulator of extracellular matrix expression and cardiac remodeling in response to pressure overload stress.
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.