DDAH1 deficiency promotes intracellular oxidative stress and cell apoptosis via a miR-21-dependent pathway in mouse embryonic fibroblasts
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- 作者：Chenyang Zhaoa ; 1 ; Tianhe Lia ; 1 ; Bingxing Hanb ; Wenhui Yuea ; Linlin Shia ; Hongyun Wanga ; Yuting Guoa ; Zhongbing Lua ; luzhongbing@ucas.ac.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：ADMA ; asymmetric dimethylarginine ; NOS ; nitric oxide synthase ; DDAH ; dimethylarginine dimethylaminohydrolase ; miRNA ; microRNA ; WT ; wild type ; KO ; knockout ; MEFs ; mouse embryonic fibroblasts ; tBHP ; tert-butyl hydroperoxide ; ROS ; reactive oxygen species ; NO ; nitric oxide ; APCs ; angiogenic progenitor cells ; SOD ; superoxide dismutase ; GSH ; reduced glutathione ; GSSG ; oxidized glutathione ; MnTBAP ; Mn(III)tetrakis (4-benzoic acid)porphyrin chloride ; tempol ; 4-Hydroxy-2 ; 2 ; 6 ; 6-tetramethylpiperidinyloxy
- 刊名：Free Radical Biology and Medicine
- 出版年：2016
- 出版时间：March 2016
- 年：2016
- 卷：92
- 期：Complete
- 页码：50-60
- 全文大小：2761 K
文摘
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DDAH1 deficiency exacerbates tBHP- and A23187-induced viability loss and apoptosis.
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DDAH1 deficiency increases oxidative stress through downregulation of SOD2.
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MiR-21 was upregulated in Ddah1−/− MEFs.
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NF-κB activation contributes to miR-21 expression in Ddah1−/− MEFs.
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Inhibition of miR-21 ameliorates apoptosis and oxidative stress in Ddah1−/− MEFs.