STAT5 mediates antiapoptotic effects of methylprednisolone on oligodendrocytes

Jan Xu, Shawei Chen, Hong Chen, Qingli Xiao, Chung Y. Hsu, Drew Michael, Jianxin Bao

研究成果: 雜誌貢獻文章同行評審

30 引文 斯高帕斯(Scopus)

摘要

Methylprednisolone (MP), a synthetic glucocorticoid agonist, is widely used for the clinical therapy of white matter diseases in the nervous system, such as spinal cord injury and multiple sclerosis. In addition to its potent anti-inflammatory and antioxidant properties, we recently discovered a selective antiapoptotic effect of MP on oligodendrocytes via the activation of the glucocorticoid receptor (GR) and the upregulation of bcl-X L, asplicing isoform of the bcl-x gene. Based on published findings of the functional interactions between GR and STAT5, a transcription factor from the family of signal transducers and activators of transcription (STAT), we examined whether the glucocorticoid signaling pathway interacts with STAT5 to upregulate bcl-X L and protect oligodendrocytes. We showherein that (1) the GR and STAT5 complex is present on the STAT5-binding site of the bcl-x promoter region in oligodendrocytes; (2) the overexpression of an activated form of STAT5 prevents a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-induced oligodendrocyte cell death; and (3) this prevention is lost when the STAT5 gene is knocked down. Thus, our results provide one molecular mechanism underlying the postinjury protective effects of oligodendrocytes by stress hormones.
原文英語
頁(從 - 到)2022-2026
頁數5
期刊Journal of Neuroscience
29
發行號7
DOIs
出版狀態已發佈 - 二月 18 2009

ASJC Scopus subject areas

  • Neuroscience(all)

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