These findings establish MG53 as a novel regulator of KChIP2 and Ito f by modulating NF-kappaB activity and reveal its critical role in electrophysiological remodeling in cardiac hypertrophy.
we are investigating the effects of hyperoxia on atrial electrophysiology using whole-cell patch-clamp electrophysiology experiments along with assessment of Kv1.5 Kv4.2 and KChIP2 transcripts and protein profiles using real-time quantitative RT-PCR and Western blotting.
the Kv4.2/KChIP2 interaction in cardiomyocytes is highly dynamic with a clear KChIP2 gene dosage effect on Kv4 channel surface expression but not on inactivation gating.
although there is a baseline presence of KChIP2 in the nucleus both in vivo and in vitro KChIP2 does not directly regulate transcriptional activity. Moreover the nuclear transport of KChIP2 is not dependent on Ca(2+). Thus KChIP2 does not function as a conventional transcription factor in the heart.
Real-time RT-PCR and Western blotting revealed that Kv4.2 expression was downregulated in both BSO-treated groups whereas KChIP2 expression was downregulated only in the H/M-Sod2(+/-)+BSO group (P<0.05).
The combined down-regulation of Kv4.2 Kv1.5 and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model.
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