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Endothelin-1 Stimulates the Expression of L-Type Ca2+ Channels in Neonatal Rat Cardiomyocytes via the Extracellular Signal–Regulated Kinase 1/2 Pathway
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Endothelin-1 Stimulates the Expression of L-Type Ca2+ Channels in Neonatal Rat Cardiomyocytes via the Extracellular Signal–Regulated Kinase 1/2 Pathway
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Endothelin-1 Stimulates the Expression of L-Type Ca2+ Channels in Neonatal Rat Cardiomyocytes via the Extracellular Signal–Regulated Kinase 1/2 Pathway
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Journal Article
Endothelin-1 Stimulates the Expression of L-Type Ca2+ Channels in Neonatal Rat Cardiomyocytes via the Extracellular Signal–Regulated Kinase 1/2 Pathway
2013
Overview
The cardiac L-type Ca
2+
channel current (
I
Ca,L
) plays an important role in controlling both cardiac excitability and excitation–contraction coupling and is involved in the electrical remodeling during postnatal heart development and cardiac hypertrophy. However, the possible role of endothelin-1 (ET-1) in the electrical remodeling of postnatal and diseased hearts remains unclear. Therefore, the present study was designed to investigate the transcriptional regulation of
I
Ca,L
mediated by ET-1 in neonatal rat ventricular myocytes using the whole-cell patch-clamp technique, quantitative RT-PCR and Western blotting. Furthermore, we determined whether the extracellular signal–regulated kinase 1/2 (ERK1/2) pathway is involved. ET-1 increased
I
Ca,L
density without altering its voltage dependence of activation and inactivation. In line with the absence of functional changes, ET-1 increased L-type Ca
2+
channel pore-forming α
1C
-subunit mRNA and protein levels without affecting the mRNA expression of auxiliary β- and α
2
/δ-subunits. Furthermore, an actinomycin D chase experiment revealed that ET-1 did not alter α
1C
-subunit mRNA stability. These effects of ET-1 were inhibited by the ET
A
receptor antagonist BQ-123 but not the ET
B
receptor antagonist BQ-788. Moreover, the effects of ET-1 on
I
Ca,L
and α
1C
-subunit expression were abolished by the ERK1/2 inhibitor (PD98059) but not by the p38 MAPK inhibitor (SB203580) or the c-Jun N-terminal kinase inhibitor (SP600125). These findings indicate that ET-1 increased the transcription of L-type Ca
2+
channel in cardiomyocytes via activation of ERK1/2 through the ET
A
receptor, which may contribute to the electrical remodeling of heart during postnatal development and cardiac hypertrophy.
Publisher
Springer-Verlag
Subject
/ Biomedical and Life Sciences
/ Enzyme Inhibitors - pharmacology
/ JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors
/ JNK Mitogen-Activated Protein Kinases - metabolism
/ Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors
/ Mitogen-Activated Protein Kinase 1 - metabolism
/ Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors
/ Mitogen-Activated Protein Kinase 3 - metabolism
/ Myocytes, Cardiac - drug effects
/ Myocytes, Cardiac - metabolism
/ Oligopeptides - pharmacology
/ Peptides, Cyclic - pharmacology
/ Rats
