These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: The effect of hypoxia-inducible factor 1-alpha on hypoxia-induced apoptosis in primary neonatal rat ventricular myocytes. Author: Zhou YF, Zheng XW, Zhang GH, Zong ZH, Qi GX. Journal: Cardiovasc J Afr; 2010; 21(1):37-41. PubMed ID: 20224844. 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.[Abstract] [Full Text] [Related] [New Search]