[The role of activation of p38 MAPK induced by LPS in TNF-alpha gene expression]

Zhonghua Yi Xue Za Zhi. 1999 May;79(5):360-4.
[Article in Chinese]

Abstract

Objective: To study the molecular mechanisms of TNF-alpha expression induced by LPS for the exploring of novel methods to prevent and treat clinical patients of endotoxic shock.

Methods: Protein kinase assay was used to detect the kinase activity stimulated by LPS; Confocal laser scan technique was used to show the translocation of p38 on the activation; RT-PCR and reporter gene system were used to study the molecular mechanism of TNF-alpha gene transcription.

Results: In RAW cells, p38 was activated on the stimulation of LPS, and activated p38 moved into nucleus from cytosol. TNF-alpha mRNA increased on the stimulation of LPS and the increased promoter transactivity induced by LPS could be inhibited significantly by specific inhibitor for p38.

Conclusion: p38 MAPK was activated on the stimulation of LPS, which brought about its translocation to the nucleus to act on transcription factors to regulate cellular processes. p38 MAPK is an important regulator of TNF-alpha gene expression induced by LPS.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Gene Transfer Techniques
  • Humans
  • Lipopolysaccharides / pharmacology*
  • Microscopy, Confocal
  • Mitogen-Activated Protein Kinases / metabolism*
  • Myocardium / cytology
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Transcription, Genetic
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / genetics
  • p38 Mitogen-Activated Protein Kinases

Substances

  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases