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论文题目: Ca2+-regulated lysosome fusion mediates angiotensin II-induced lipid raft clustering in mesenteric endothelial cells
英文论文题目: Ca2+-regulated lysosome fusion mediates angiotensin II-induced lipid raft clustering in mesenteric endothelial cells
第一作者: Han, WQ; Chen, WD; Zhang, K; Liu, JJ; Wu, YJ; Gao, PJ
英文第一作者: Han, WQ; Chen, WD; Zhang, K; Liu, JJ; Wu, YJ; Gao, PJ
联系作者: Gao, PJ (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Shanghai, Peoples R China.
英文联系作者: Gao, PJ (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Shanghai, Peoples R China.
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发表年度: 2016
卷: 39
期: 4
页码: 227-236
摘要: It has been reported that intracellular Ca2+ is involved in lysosome fusion and membrane repair in skeletal cells. Given that angiotensin II (Ang II) elicits an increase in intracellular Ca2+ and that lysosome fusion is a crucial mediator of lipid raft (LR) clustering, we hypothesized that Ang II induces lysosome fusion and activates LR formation in rat mesenteric endothelial cells (MECs). We found that Ang II acutely increased intracellular Ca2+ content, an effect that was inhibited by the extracellular Ca2+ chelator ethylene glycol tetraacetic acid (EGTA) and the inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release inhibitor 2-aminoethoxydiphenyl borate (2-APB). Further study showed that EGTA almost completely blocked Ang II-induced lysosome fusion, the translocation of acid sphingomyelinase (ASMase) to LR clusters, ASMase activation and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase activation. In contrast, 2-APB had a slight inhibitory effect. Functionally, both the lysosome inhibitor bafilomycin A1 and the ASMase inhibitor amitriptyline reversed Ang II-induced impairment of vasodilation. We conclude that Ca2+-regulated lysosome fusion mediates the Ang II-induced regulation of the LR-redox signaling pathway and mesenteric endothelial dysfunction.
英文摘要: It has been reported that intracellular Ca2+ is involved in lysosome fusion and membrane repair in skeletal cells. Given that angiotensin II (Ang II) elicits an increase in intracellular Ca2+ and that lysosome fusion is a crucial mediator of lipid raft (LR) clustering, we hypothesized that Ang II induces lysosome fusion and activates LR formation in rat mesenteric endothelial cells (MECs). We found that Ang II acutely increased intracellular Ca2+ content, an effect that was inhibited by the extracellular Ca2+ chelator ethylene glycol tetraacetic acid (EGTA) and the inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release inhibitor 2-aminoethoxydiphenyl borate (2-APB). Further study showed that EGTA almost completely blocked Ang II-induced lysosome fusion, the translocation of acid sphingomyelinase (ASMase) to LR clusters, ASMase activation and NADPH (nicotinamide adenine dinucleotide phosphate) oxidase activation. In contrast, 2-APB had a slight inhibitory effect. Functionally, both the lysosome inhibitor bafilomycin A1 and the ASMase inhibitor amitriptyline reversed Ang II-induced impairment of vasodilation. We conclude that Ca2+-regulated lysosome fusion mediates the Ang II-induced regulation of the LR-redox signaling pathway and mesenteric endothelial dysfunction.
刊物名称: HYPERTENSION RESEARCH
英文刊物名称: HYPERTENSION RESEARCH
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学科: Peripheral Vascular Disease
英文学科: Peripheral Vascular Disease
影响因子: 3.581
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论文类别: Article
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