Abstract
In the present study we characterized a "crosstalk" mechanism between transforming growth factor beta-1 (TGF β-1) and endothelin-1 (ET1) signaling pathways in neonatal cardiac myocytes. A 5 minute pretreatment with 1 ng/ml concentrations of TGF β-1 attenuated ET1-induced negative chronotropic effects and translocation of the α, δ and εPKC isozymes to the particulate cell fraction. We found no effect of TGF β-1 on responses induced by the P2 purinergic agonist ATP or phorbol ester. Treatment of cardiac myocytes with acidic fibroblast growth factor (aFGF) did not alter ET1- or ATP-mediated effects on contraction rate or translocation of PKC isozymes to the particulate fraction. Our studies suggest that TGF β-1 may act as a negative modulator of ET1- but not ATP- or phorbol ester-induced PKC isozyme signaling events in neonatal cardiac myocytes. A better understanding of the complex ET1 and TGF β-1 signaling mechanisms in neonatal heart cells should enhance our knowledge regarding the interplay between these pathways.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 99-113 |
| Number of pages | 15 |
| Journal | Life sciences |
| Volume | 71 |
| Issue number | 1 |
| DOIs | |
| State | Published - May 24 2002 |
Keywords
- Cardiac myocytes
- Contraction
- Crosstalk
- Endothelin-1
- P-purinergic
- PKC
- Phorbol
- TGF β-1
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)