| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1930813 | Biochemical and Biophysical Research Communications | 2011 | 5 Pages |
Transforming growth factor β (TGF-β) signaling plays an important role in the pathogenesis of cardiac hypertrophy. However, the molecular mechanism of TGF-β signaling during the process of cardiac remodeling remains poorly understood. In the present study, by employing single-molecule fluorescence imaging approach, we demonstrated that in neonatal rat cardiomyocytes, TGF-β type II receptors (TβRII) existed as monomers at the low expression level, and dimerized upon TGF-β1 stimulation. Importantly, for the first time, we found the increased dimerization of TβRII in hypertrophic cardiomyocytes comparing to the normal cardiomyocytes. The enhanced TβRII dimerization was correlated with the enhanced Smad3 phosphorylation levels. These results provide new information on the mechanism of TGF-β signaling in cardiac remodeling.
► TGF-β type II receptors (TβRII) existed as monomers at the low expression level, and dimerized upon TGF-β1 stimulation in neonatal rat cardiomyocytes. ► TβRII dimerization was enhanced in hypertrophic cardiomyocytes comparing to the normal cardiomyocytes. ► The hypertrophic cardiomyocytes with enhanced TβRII dimerization exhibited a higher phosphorylation level of Smad3.
