Full text is available at the source.
Notch signaling may block heart scar cells from changing by opposing TGF-β1/Smad3 signals
Updated
Abstract
TGF-β1 increased collagen I secretion and myofibroblast marker expression in cardiac fibroblasts.
- TGF-β1 decreased fibroblast marker expression while increasing myofibroblast markers in rat cardiac fibroblasts.
- TGF-β1 enhanced proliferation, invasion, and adhesion of cardiac fibroblasts.
- N1ICD overexpression inhibited the effects of TGF-β1 on cardiac fibroblast behavior.
- N1ICD knockdown led to increased phosphorylation of Smad3 in cardiac fibroblasts.
- N1ICD and Smad3 were shown to interact and colocalize in the nuclei of cardiac fibroblasts.
- Notch signaling is associated with the inhibition of myocardial fibrosis, while TGF-β1/Smad3 signaling promotes it.
Simplified