Notch3/Akt signaling contributes to OSM-induced protection against cardiac ischemia/reperfusion injury

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• 作者：Mingming Zhang ; Chen Wang ; Jianqiang Hu ; Jie Lin ; Zhijing Zhao ; Min Shen…
• 关键词：Oncostatin M ; OSM ; Notch3 ; Ischemia/reperfusion injury ; I/R injury ; Mitochondria
• 刊名：Apoptosis
• 出版年：2015
• 出版时间：September 2015
• 年：2015
• 卷：20
• 期：9
• 页码：1150-1163
• 全文大小：14,307 KB
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• 作者单位：Mingming Zhang (1)
  Chen Wang (1)
  Jianqiang Hu (1)
  Jie Lin (1)
  Zhijing Zhao (1)
  Min Shen (1)
  Haokao Gao (1)
  Na Li (1)
  Min Liu (1)
  Pengfei Zheng (1)
  Cuiting Qiu (1)
  Erhe Gao (2)
  Haichang Wang (1)
  Dongdong Sun (1)
  
  1. Department of Cardiology, Xijing Hospital, Fourth Military Medical University, 127 West Changle Road, Xi’an, 710032, Shaanxi, China
  2. Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA, USA
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Oncology
  Cancer Research
  Cell Biology
  Biochemistry
  Virology
  
• 出版者：Springer Netherlands
• ISSN：1573-675X

文摘

Oncostatin M (OSM) exhibits many unique biological activities by activating the Oβ receptor. However, its role in myocardial ischemia/reperfusion injury (I/R injury) in mice remains unknown. We investigated whether Notch3/Akt signaling is involved in the regulation of OSM-induced protection against cardiac I/R injury. The effects of OSM were assessed in mice that underwent myocardial I/R injury by OSM treatment or by genetic deficiency of the OSM receptor Oβ. We investigated its effects on cardiomyocyte apoptosis and mitochondrial biogenesis and whether Notch3/Akt signaling was involved in the regulation of OSM-induced protection against cardiac I/R injury. The mice underwent 30?min of ischemia followed by 3?h of reperfusion and were randomized to be treated with Notch3 siRNA (siNotch3) or lentivirus carrying Notch3 cDNA (Notch3) 72?h before coronary artery ligation. Myocardial infarct size, cardiac function, cardiomyocyte apoptosis and mitochondria morphology in mice that underwent cardiac I/R injury were compared between groups. OSM alleviated cardiac I/R injury by inhibiting cardiomyocyte apoptosis through promotion of Notch3 production, thus activating the PI3K/Akt pathway. OSM enhanced mitochondrial biogenesis and mitochondrial function in mice subjected to cardiac I/R injury. In contrast, OSM receptor Oβ knock out exacerbated cardiac I/R injury, decreased Notch3 production, enhanced cardiomyocyte apoptosis, and impaired mitochondrial biogenesis in cardiac I/R injured mice. The mechanism of OSM on cardiac I/R injury is partly mediated by the Notch3/Akt pathway. These results suggest a novel role of Notch3/Akt signaling that contributes to OSM-induced protection against cardiac I/R injury.