兰尼定受体
线粒体
钌红
Uniporter公司
内质网
细胞凋亡
橙皮苷
化学
细胞生物学
程序性细胞死亡
分子生物学
生物化学
生物
钙
胞浆
病理
有机化学
酶
替代医学
医学
作者
Silvia Yumnam,Gyeong Eun Hong,Suchismita Raha,Gon Sup Kim,Ho Jeong Lee,Won‐Sup Lee,Eunhee Kim,Gon Sup Kim
摘要
Paraptosis is a programmed cell death which is morphologically and biochemically different from apoptosis. In this study, we have investigated the role of Ca 2+ in hesperidin‐induced paraptotic cell death in HepG2 cells. Increase in mitochondrial Ca 2+ level was observed in hesperidin treated HepG2 cells but not in normal liver cancer cells. Inhibition of inositol‐1,4,5‐triphosphate receptor (IP 3 R) and ryanodine receptor also block the mitochondrial Ca 2+ accumulation suggesting that the release of Ca 2+ from the endoplasmic reticulum (ER) may probably lead to the increase in mitochondrial Ca 2+ level. Pretreatment with ruthenium red (RuRed), a Ca 2+ uniporter inhibitor inhibited the hesperidin‐induced mitochondrial Ca 2+ overload, swelling of mitochondria, and cell death in HepG2 cells. It has also been demonstrated that mitochondrial Ca 2+ influxes act upstream of ROS and mitochondrial superoxide production. The increased ROS production further leads to mitochondrial membrane loss in hesperidin treated HepG2 cells. Taken together our results show that IP 3 R and ryanodine receptor mediated release of Ca 2+ from the ER and its subsequent influx through the uniporter into mitochondria contributes to hesperidin‐induced paraptosis in HepG2 cells. J. Cell. Physiol. 231: 1261–1268, 2016. © 2015 Wiley Periodicals, Inc.
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