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• W2016460839 abstract "Hypertrophied myocardium is associated with reductions in the transient outward K + current ( I to) and expression of pore-forming Kv4.2/4.3 and auxiliary KChIP2 subunits. Here we show that KChIP2 mRNA and protein levels are dramatically decreased to 10% to 30% of control levels in the left ventricle of aorta-constricted rats in vivo and phenylephrine (PE)-treated myocytes in vitro. PE also markedly decreases I to density. Inhibition of protein kinase Cs (PKCs) does not affect the PE-induced reduction in KChIP2 mRNA level, whereas activation of PKC with phorbol ester (phorbol myristate [PMA]) causes a marked reduction in KChIP2 mRNA level. Pharmacological inhibition of MEKs or overexpression of a dominant-negative MEK1 increases the basal KChIP2 mRNA expression and blocks the PMA-induced decrease in auxiliary subunit mRNA level. In addition, a constitutively active MEK1 decreases the basal KChIP2 mRNA level, and PMA causes no further reduction in auxiliary subunit mRNA level in active MEK1-expressing cells. Furthermore, pharmacological inhibition of JNKs or overexpression of a dominant-negative JNK1 prevents the PE-induced, but not PMA-induced, reduction in KChIP2 mRNA expression. These results suggest that downregulation of KChIP2 expression significantly contributes to the hypertrophy-associated reduction in I to density. They also indicate that the expression of KChIP2 mRNA is controlled by the 2 branches of mitogen-activated protein kinase pathways: JNKs play a predominant role in mediating the PE-induced reduction, whereas the MEK-ERK pathway influences the basal expression and mediates the PKC-mediated downregulation." @default.
• W2016460839 created "2016-06-24" @default.
• W2016460839 creator A5091318694 @default.
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• W2016460839 date "2006-02-17" @default.
• W2016460839 modified "2023-10-03" @default.
• W2016460839 title "Mitogen-Activated Protein Kinases Control Cardiac KChIP2 Gene Expression" @default.
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• W2016460839 doi "https://doi.org/10.1161/01.res.0000201956.86258.e1" @default.
• W2016460839 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1373668" @default.
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