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缺氧诱导因子1-α对原代新生大鼠心室肌细胞缺氧诱导凋亡的影响。

The effect of hypoxia-inducible factor 1-alpha on hypoxia-induced apoptosis in primary neonatal rat ventricular myocytes.

作者信息

Zhou Yan-Fang, Zheng Xiao-Wei, Zhang Guo-Hui, Zong Zhi-Hong, Qi Guo-Xian

机构信息

Department of Cardiology, First Affiliated Hospital of China Medical University, Shenyang, China.

出版信息

Cardiovasc J Afr. 2010 Jan-Feb;21(1):37-41.

DOI:
PMID:20224844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3721275/
Abstract

AIM: To study the role of hypoxia-inducible factor 1-alpha (HIF-1alpha) on hypoxia-induced apoptosis in primary neonatal rat ventricular myocytes. METHODS: Primary neonatal rat ventricular myocytes were exposed to hypoxia for 24 hours. HIF-1alpha activity was suppressed by treating the cells with 3-(5'-hydroxymethyl-2'- furyl)-1-benzyl indazole (YC-1). The degree of cell apoptosis was assessed by Hoechst 33258 DNA staining. The levels of HIF-1alpha and the pro-apoptotic proteins Bnip3, Bax and Bad were measured with western blotting. RESULTS: On exposure to hypoxia, there was an increase in the expression levels of HIF-1alpha, and the pro-apoptotic protein Bnip3 was upregulated. Suppression of HIF-1alpha activity by YC-1 treatment was followed by blockade of hypoxia-induced apoptosis and Bnip3 expression; however, the changes in the levels of Bax and Bad expression were unclear. CONCLUSION: Acute hypoxia enhanced primary neonatal rat ventricular myocyte apoptosis through the activation of HIF-1alpha and a mechanism that perhaps involved Bnip3. Targeting HIF-1alpha may be a new strategy for reducing the degree of hypoxia-induced apoptosis in ventricular myocytes.

摘要

目的：研究缺氧诱导因子1α（HIF-1α）在新生大鼠原代心室肌细胞缺氧诱导凋亡中的作用。 方法：将新生大鼠原代心室肌细胞暴露于缺氧环境24小时。用3-（5'-羟甲基-2'-呋喃基）-1-苄基吲唑（YC-1）处理细胞以抑制HIF-1α活性。通过Hoechst 33258 DNA染色评估细胞凋亡程度。用蛋白质免疫印迹法检测HIF-1α以及促凋亡蛋白Bnip3、Bax和Bad的水平。 结果：暴露于缺氧环境时，HIF-1α的表达水平升高，促凋亡蛋白Bnip3上调。用YC-1处理抑制HIF-1α活性后，缺氧诱导的凋亡和Bnip3表达被阻断；然而，Bax和Bad表达水平的变化不明确。 结论：急性缺氧通过激活HIF-1α以及可能涉及Bnip3的机制增强新生大鼠原代心室肌细胞凋亡。靶向HIF-1α可能是降低心室肌细胞缺氧诱导凋亡程度的新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/31c89f212b14/cvja-21-40-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/9e8ae6120118/cvja-21-38-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/c1e21a48dbdf/cvja-21-39-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/530713128a13/cvja-21-39-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/9ea85586c540/cvja-21-40-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/31c89f212b14/cvja-21-40-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/9e8ae6120118/cvja-21-38-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/c1e21a48dbdf/cvja-21-39-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/530713128a13/cvja-21-39-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/9ea85586c540/cvja-21-40-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ce5/3721275/31c89f212b14/cvja-21-40-g005.jpg

相似文献

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引用本文的文献

[1]
Mitochondrial Dysfunction and Changes in High-Energy Compounds in Different Cellular Models Associated to Hypoxia: Implication to Schizophrenia.

Sci Rep. 2019-12-2

[2]
FOXO3a regulates BNIP3 and modulates mitochondrial calcium, dynamics, and function in cardiac stress.

Am J Physiol Heart Circ Physiol. 2016-12-1

[3]
Overexpression of CyclinA2 ameliorates hypoxia-impaired proliferation of cardiomyocytes.

Exp Ther Med. 2014-11

[4]
Apelin-APJ effects of ginsenoside-Rb1 depending on hypoxia-induced factor 1α in hypoxia neonatal cardiomyocytes.

Chin J Integr Med. 2014-6-3

[5]
Molecular mechanisms of action and therapeutic uses of pharmacological inhibitors of HIF-prolyl 4-hydroxylases for treatment of ischemic diseases.

Antioxid Redox Signal. 2014-6-1

[6]
Mild hypoxia-induced cardiomyocyte hypertrophy via up-regulation of HIF-1α-mediated TRPC signalling.

J Cell Mol Med. 2012-9

[7]
Disruption of hypoxia-inducible transcription factor-prolyl hydroxylase domain-1 (PHD-1-/-) attenuates ex vivo myocardial ischemia/reperfusion injury through hypoxia-inducible factor-1α transcription factor and its target genes in mice.

Antioxid Redox Signal. 2011-4-8

本文引用的文献

[1]
BNIP3 mediates cell death by different pathways following localization to endoplasmic reticulum and mitochondrion.

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Hypoxia inhibits paclitaxel-induced apoptosis through adenosine-mediated phosphorylation of bad in glioblastoma cells.

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Proc Natl Acad Sci U S A. 2002-10-1

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