Transforming growth factor beta-1 attenuates endothelin-1-induced functions in neonatal cardiac myocytes

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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 languageEnglish (US)
Pages (from-to)99-113
Number of pages15
JournalLife sciences
Volume71
Issue number1
DOIs
StatePublished - May 24 2002

Fingerprint

Endothelin-1
Cardiac Myocytes
Transforming Growth Factor beta
Isoenzymes
Adenosine Triphosphate
Phorbol Esters
Purinergic Agonists
Fibroblast Growth Factor 1
Crosstalk
Modulators

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)

Cite this

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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.",
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N2 - 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.

AB - 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.

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KW - TGF β-1

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