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Anti‐apoptotic protein survivin plays a significant role in tubular morphogenesis of human coronary arteriolar endothelial cells by hypoxic preconditioning
Author(s) -
Zhu Li,
Fukuda Shoji,
Cordis Gerald,
Das Dipak K,
Maulik Nilanjana
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03084-8
Subject(s) - survivin , microbiology and biotechnology , morphogenesis , kinase , ly294002 , apoptosis , protein kinase b , hypoxia (environmental) , biology , pi3k/akt/mtor pathway , chemistry , phosphatidylinositol , signal transduction , biochemistry , oxygen , organic chemistry , gene
Brief exposure of endothelial cells to oxidative stress induced by hypoxia followed by reoxygenation enhances tube formation. Our study provides evidence that hypoxic preconditioning accelerates tubular morphogenesis along with the activation of reactive oxygen species‐inducible nuclear transcription factor‐κB (NF‐κB), phosphatidylinositol 3‐kinase (PI3‐kinase) and broad‐spectrum anti‐apoptotic protein survivin in human coronary arteriolar endothelial cells (HCAEC). The formation of tubular morphogenesis was inhibited by using the PI3‐kinase and NF‐κB antagonists LY294002 and SN50 respectively. The activation of survivin by hypoxic preconditioning was also inhibited by LY294002 and SN50 along with increased apoptosis in HCAEC. These data demonstrate a crucial role of PI3‐kinase/Akt/NF‐κB/survivin signaling in tubular morphogenesis of HCAEC triggered by hypoxic preconditioning.