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胰岛素样生长因子-1通过PI3K/Akt信号通路对新生心肌细胞中I(K)和I(K1)通道的影响

Effects of IGF-1 on I(K) and I(K1) Channels via PI3K/Akt Signaling in Neonatal Cardiac Myocytes.

作者信息

Millis Richard M, Alvin Zikiar V, Zhao Aiqiu, Haddad Georges E

机构信息

Department of Physiology & Biophysics, College of Medicine, Howard University, Washington, DC 20059, USA.

出版信息

Int J Cell Biol. 2012;2012:712153. doi: 10.1155/2012/712153. Epub 2012 Jun 18.

DOI:10.1155/2012/712153
PMID:22761619
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3385609/
Abstract

Previous studies suggest that sarcolemmal potassium currents play important roles in cardiac hypertrophy. IGF-1 contributes to cardiac hypertrophy via activation of PI3K/Akt signaling. However, the relationships between IGF-1, PI3K/Akt signaling and sarcolemmal potassium currents remain unknown. Therefore, we tested the hypothesis that IGF-1 and PI3K/Akt signaling, independently, decrease sarcolemmal potassium currents in cardiac myocytes of neonatal rats. We compared the delayed outward rectifier (I(K)) and the inward rectifier (I(K)) current densities resulting from IGF-1 treatments to those resulting from simulation of PI3K/Akt signaling using adenoviral (Ad) BD110 and wild-type Akt and to those resulting from inhibition of PI3K signaling by LY294002. Ad.BD110 and Ad.Akt decreased I(K) and these decrements were attenuated by LY 294002. The IGF-1 treatments decreased both I(K) and I(K1) but only the I(K) decrement was attenuated by LY294002. These findings demonstrate that IGF-1 may contribute to cardiac hypertrophy by PI3K/Akt signal transduction mechanisms in neonatal rat cardiomyocytes. Failure of LY294002 to effectively antagonize IGF-1 induced decrements in I(K1) suggests that a signal pathway adjunct to PI3K/Akt contributes to IGF-1 protection against arrhythmogenesis in these myocytes. Our findings imply that sarcolemmal outward and inward rectifier potassium channels are substrates for IGF-1/PI3K/Akt signal transduction molecules.

摘要

先前的研究表明，肌膜钾电流在心肌肥大中起重要作用。胰岛素样生长因子-1（IGF-1）通过激活PI3K/Akt信号通路促进心肌肥大。然而，IGF-1、PI3K/Akt信号通路与肌膜钾电流之间的关系尚不清楚。因此，我们验证了以下假设：IGF-1和PI3K/Akt信号通路分别降低新生大鼠心肌细胞的肌膜钾电流。我们比较了IGF-1处理导致的延迟外向整流钾电流（I(K)）和内向整流钾电流（I(K1)）密度，与使用腺病毒（Ad）BD110和野生型Akt模拟PI3K/Akt信号通路导致的电流密度，以及LY294002抑制PI3K信号通路导致的电流密度。Ad.BD110和Ad.Akt降低了I(K)，而LY294002减弱了这些降低。IGF-1处理降低了I(K)和I(K1)，但只有I(K)的降低被LY294002减弱。这些发现表明，IGF-1可能通过PI3K/Akt信号转导机制在新生大鼠心肌细胞中促进心肌肥大。LY294002未能有效拮抗IGF-1诱导的I(K1)降低，表明PI3K/Akt信号通路之外的信号通路有助于IGF-1对这些心肌细胞心律失常的保护作用。我们的发现意味着肌膜外向和内向整流钾通道是IGF-1/PI3K/Akt信号转导分子的作用底物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5edc/3385609/e69cfb19ecf6/IJCB2012-712153.008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5edc/3385609/7ddbbbd61c2c/IJCB2012-712153.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5edc/3385609/1bd5101390d1/IJCB2012-712153.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5edc/3385609/7f17d0a59a30/IJCB2012-712153.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5edc/3385609/e69cfb19ecf6/IJCB2012-712153.008.jpg

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