IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科
学科主题临床医学
Novel anti-oxidative role of calreticulin in protecting A549 human type II alveolar epithelial cells against hypoxic injury
Jia, Lingyun2; Xu, Mingjiang1; Zhen, Wei1; Shen, Xun3; Zhu, Yi1; Wang, Wang2; Wang, Xian1,2
关键词Cellular Protection Hypoxic Injury Calreticulin Thioredoxin Reactive Oxygen Species
刊名AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
2008
DOI10.1152/ajpcell.00019.2007
294期:1页:C47-C55
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Physiology
研究领域[WOS]Cell Biology ; Physiology
关键词[WOS]ENDOPLASMIC-RETICULUM STRESS ; ISCHEMIC PRECONDITIONING PROTECTS ; OXIDATIVE STRESS ; HEAT-SHOCK ; CALCIUM IONOPHORE ; INDUCED APOPTOSIS ; DEATH ; THIOREDOXIN ; EXPRESSION ; KINASE
英文摘要

Short-term hypoxic pretreatment is an effective approach to protect the lung from subsequent prolonged hypoxic injury under conditions such as lung transplantation, shock, and trauma. However, the signaling pathways are not well understood. By use of high-throughput, two-dimensional electrophoresis combined with mass spectrometry, we found that short-term hypoxic treatment upregulated calreticulin (CRT), an endoplasmic-reticulum stress protein, in A549 human type II alveolar epithelial cells. Genetic manipulation of CRT expression in A549 cells through small interferring RNA inhibition or overexpression demonstrated a positive correlation between CRT expression level and cell viability in subsequent prolonged hypoxia, which indicates that CRT is a key mediator of short-term hypoxia-induced cell protection. Importantly, CRT overexpression prevented reactive oxygen species (ROS) accumulation during prolonged hypoxia by inducing the expression of thioredoxin (TRX), an antioxidant, in A549 cells. Furthermore, CRT promoted the nuclear translocation of nuclear factor-E2-related factor 2, the transcription factor of TRX. Finally, overexpressing an inactive TRX mutant reversed the effects of CRT on ROS accumulation and cell protection. Our results demonstrate that CRT stimulates the anti-oxidant pathway and contributes to short-term hypoxia-induced protection in A549 type II alveolar epithelial cells, which may have potential therapeutic ramifications for hypoxic pulmonary diseases.

语种英语
WOS记录号WOS:000252507600007
Citation statistics
Cited Times:21[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56261
Collection北京大学第三临床医学院_心血管内科
作者单位1.Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr,Minist Edut, Sch Basic Med Sci,Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
2.Peking Univ, Third Hosp, Inst Vasc Med, Beijing 100083, Peoples R China
3.Chinese Acad Sci, Inst Biophys, Beijing 100080, Peoples R China
Recommended Citation
GB/T 7714
Jia, Lingyun,Xu, Mingjiang,Zhen, Wei,et al. Novel anti-oxidative role of calreticulin in protecting A549 human type II alveolar epithelial cells against hypoxic injury[J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY,2008,294(1):C47-C55.
APA Jia, Lingyun.,Xu, Mingjiang.,Zhen, Wei.,Shen, Xun.,Zhu, Yi.,...&Wang, Xian.(2008).Novel anti-oxidative role of calreticulin in protecting A549 human type II alveolar epithelial cells against hypoxic injury.AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY,294(1),C47-C55.
MLA Jia, Lingyun,et al."Novel anti-oxidative role of calreticulin in protecting A549 human type II alveolar epithelial cells against hypoxic injury".AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 294.1(2008):C47-C55.
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