Intact mitochondrial Ca²⁺ uniport is essential for agonist-induced activation of endothelial nitric oxide synthase (eNOS)

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• 作者：Suphachai Charoensin^a ; Emrah Eroglu^a ; Marissa Opelt^b ; Helmut Bischof^a ; Corina T. Madreiter-Sokolowski^a ; Andrijana Kirsch^a ; Maria R. Depaoli^a ; Sa&scaron ; a Frank^a ; Astrid Schrammel^b ; Bernd Mayer^b ; Markus Waldeck-Weiermair^a ; Wolfgang F. Graier^a ; Roland Malli^a ; ^{roland.malli@medunigraz.at}
• 关键词：Ψmito ; mitochondrial membrane potential ; EMRE ; essential mitochondrial calcium uniporter regulator ; eNOS ; endothelial nitric oxide synthase ; geNOps ; genetically encoded fluorescent nitric oxide probes ; EGFP ; enhanced green fluorescent protein ; ER ; endoplasmic reticulum ; IP3 ; inositol 1 ; 4 ; 5-trisphosphate ; MCU ; mitochondrial calcium uniporter ; MICU1 ; mitochondrial calcium uptake 1 ; NO&bull ; nitric oxide ; P-eNOS ; phosphorylated endothelial nitric oxide synthase ; RFP ; red fluorescent protein ; SOCE
• 刊名：Free Radical Biology and Medicine
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：102
• 期：Complete
• 页码：248-259
• 全文大小：1932 K
• 卷排序：102

文摘

geNOps allow real-time imaging of eNOS-mediated NO formation in single cells. Impairment of mitochondrial Ca2+ uptake reduces NO synthesis by eNOS. Increased mitochondrial Ca2+ uptake facilitates Ca2+-triggered NO formation. Mitochondrial Ca2+ uptake does not affect eNOS phosphorylation. The link between mitochondria and eNOS activity remains unidentified.