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Effects of long-term intermittent hypoxia on mitochondrial and Fas death receptor dependent apoptotic pathways in rat hearts.

Abstract：

BACKGROUND:It is unclear whether the cardiac mitochondrial dependent apoptotic pathways and Fas death receptor dependent apoptotic pathways will be induced by long-term intermittent hypoxia. METHODS:Twenty-seven Sprague-Dawley rats were randomly assigned into three groups: normoxia, long-term intermittent hypoxia (12% O(2), 8 h/day) for 4 weeks (4WLTIH) and for 8 weeks (8WLTIH). Histological analysis, Western blotting and RT-PCR in the three groups were performed on tissue from the excised left ventricle. RESULTS:Mitochondrial dependent pro-apoptotic pathway, BNIP3, caspase 9, and caspase 3, and the Fas death receptor dependent pro-apoptotic pathway, Fas, caspase 8, and caspase 3 were all significantly increased after 4WLTIH and even further enhanced after 8WLTIH. In addition, mitochondrial related anti-apoptotic proteins, Bcl2, its upstream phosphorylated protein kinase B (Akt), and the mitochondrial key oxidative enzyme, cytochrome c oxidase, were all decreased after 4WLTIH and further reduced after 8WLTIH. CONCLUSIONS:The mitochondrial dependent apoptotic pathways and Fas death receptor dependent apoptotic pathways in rat hearts were both activated by long-term intermittent hypoxia.

journal_name

Int J Cardiol

journal_title

International journal of cardiology

authors

Lee SD,Kuo WW,Lin JA,Chu YF,Wang CK,Yeh YL,Wang SG,Liu JY,Chang MH,Huang CY

doi

10.1016/j.ijcard.2006.03.064

subject

Has Abstract

pub_date

2007-04-04 00:00:00

pages

348-56

issue

3

eissn

0167-5273

issn

1874-1754

pii

S0167-5273(06)00476-1

journal_volume

116

pub_type

杂志文章

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