Oxidative stress-induced apoptotic insults to rat osteoblasts are attenuated by nitric oxide pretreatment via GATA-5-involved regulation of Bcl-X

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• 作者：Gong-Jhe Wu ; Weu Wang ; Yi-Ling Lin ; Shing Hwa Liu ; Ruei-Ming Chen
• 关键词：Osteoblasts ; Oxidative stress ; Nitric oxide ; GATA ; 5 ; Apoptosis ; Bcl ; XL
• 刊名：Archives of Toxicology
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：90
• 期：4
• 页码：905-916
• 全文大小：967 KB
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• 作者单位：Gong-Jhe Wu (1) (2)
  Weu Wang (3)
  Yi-Ling Lin (4)
  Shing Hwa Liu (5)
  Ruei-Ming Chen (2) (4) (6)
  
  1. Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan
  2. Anesthetics and Toxicology Research Center, Taipei Medical University Hospital, Taipei, Taiwan
  3. Division of General Surgery, Department of Surgery, Taipei Medical University Hospital, Taipei, Taiwan
  4. Cell Physiology and Molecular Image Research Center, Wan-Fang Hospital, Taipei Medical University, Taipei, Taiwan
  5. Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan
  6. Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 250 Wu-Hsing St., Taipei, 110, Taiwan
  
• 刊物主题：Pharmacology/Toxicology; Occupational Medicine/Industrial Medicine; Environmental Health; Biomedicine general;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-0738

文摘

Nitric oxide (NO) has biphasic effects on regulating osteoblast survival and death. This study was aimed to evaluate the effects of NO pretreatment on hydrogen peroxide (HP)-induced insults of rat osteoblasts and the possible mechanisms. Exposure of osteoblasts prepared from rat calvarias to HP significantly increased intracellular reactive oxygen species levels, decreased alkaline phosphatase activity and cell survival, and ultimately induced cell apoptosis. However, NO pretreatment lowered HP-induced oxidative stress and apoptotic insults. In parallel, HP increased Bax levels and its translocation from the cytoplasm to mitochondria. NO pretreatment caused significant attenuations in HP-induced modulations in Bax synthesis and translocation. In contrast, pretreatment with NO enhanced levels and translocation of antiapoptotic Bcl-X_L protein in rat osteoblasts. RNA analyses further revealed that HP inhibited Bcl-X_L mRNA expression without affecting Bax mRNA levels. In comparison, NO induced Bcl-X_L mRNA production and alleviated HP-caused inhibition of this mRNA expression. As to the mechanism, HP suppressed RNA and protein levels of transcription factor GATA-5 in rat osteoblasts. Pretreatment with NO induced GATA-5 mRNA and protein expressions and simultaneously attenuated HP-induced inhibition of this gene’s expression. Consequently, GATA-5 knockdown using RNA interference inhibited Bcl-X_L mRNA expression and concurrently lowered NO’s protection against HP-induced apoptotic insults. Therefore, this study showed that NO can protect rat osteoblasts from HP-induced apoptotic insults. The protective mechanisms are mediated by GATA-5-mediated transcriptional induction of Bcl-X _L gene, and translocational modulation of Bcl-X_L and Bax proteins.