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- W2023013068 abstract "In the present study we characterized a crosstalk mechanism between transforming growth factor beta-1 (TGF beta-1) and endothelin-1 (ET1) signaling pathways in neonatal cardiac myocytes. A 5 minute pretreatment with 1 ng/ml concentrations of TGF beta-1 attenuated ET1-induced negative chronotropic effects and translocation of the alpha, delta and varepsilonPKC isozymes to the particulate cell fraction. We found no effect of TGF beta-1 on responses induced by the P(2) 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 beta-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 beta-1 signaling mechanisms in neonatal heart cells should enhance our knowledge regarding the interplay between these pathways." @default.
- W2023013068 created "2016-06-24" @default.
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- W2023013068 date "2002-05-01" @default.
- W2023013068 modified "2023-10-17" @default.
- W2023013068 title "Transforming growth factor beta-1 attenuates endothelin-1-induced functions in neonatal cardiac myocytes" @default.
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- W2023013068 doi "https://doi.org/10.1016/s0024-3205(02)01624-7" @default.
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