Suppression of rat Frizzled-2 attenuates hypoxia/reoxygenation-induced Ca²⁺ accumulation in rat H9c2 cells

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• 作者：Shan-shan Zhou ; Fei He ; Ai-hua Chen ; ^{zj_chenaihua@126.com} ; Pei-yuan Hao ; Xu-dong Song
• 关键词：Frizzled-2 ; H9c2(2-1) cells ; Hypoxia/reoxygenation ; Calcium ; Ischemia-reperfusion injury
• 刊名：Experimental Cell Research
• 出版年：2012
• 出版时间：1 August, 2012
• 年：2012
• 卷：318
• 期：13
• 页码：1480-1491
• 全文大小：1639 K

文摘

Growing evidence suggests that Ca²⁺ overload is one of the major contributors of myocardial ischemia/reperfusion-induced injury. Since Frizzled-2 receptor, a seven transmembrane protein, transduces downstream signaling by specialized binding of Wnt5a to increase intracellular Ca²⁺ release, this work aimed to investigate the effect of Frizzled-2 on Ca²⁺ accumulation in H9c2 cells, which were subjected to hypoxia/reoxygenation to mimic myocardial ischemia/reperfusion. After exposing H9c2 cells to hypoxia/reoxygenation, we observed higher expression of Frizzled-2 and Wnt5a as compared to control group cells. Hypoxia/reoxygenation-induced intracellular Ca²⁺ accumulation approached that of cells transfected with frizzled-2 plasmid. In cells treated with RNAi specifically designed against frizzled-2, intracellular Ca²⁺ in both hypoxia/reoxygenation-treated cells and plasmid-treated cells were decreased. Rats that underwent ischemia/reperfusion injury exhibited increased intracellular Ca²⁺ with high expression levels of Frizzled-2 and Wnt5a as compared to the sham group. Our data indicates that upon binding to Wnt5a, increased Frizzled-2 expression after hypoxia/reoxygenation treatment activated intracellular calcium release in H9c2 cells. Our findings provide a new perspective in understanding calcium overload in myocardial ischemia/reperfusion.