Zhou Yan-Fang, Zheng Xiao-Wei, Zhang Guo-Hui, Zong Zhi-Hong, Qi Guo-Xian
Department of Cardiology, First Affiliated Hospital of China Medical University, Shenyang, China.
Cardiovasc J Afr. 2010 Jan-Feb;21(1):37-41.
To study the role of hypoxia-inducible factor 1-alpha (HIF-1alpha) on hypoxia-induced apoptosis in primary neonatal rat ventricular myocytes.
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.
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.
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.
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。
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。
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。
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。
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