[TNF-α induces the release of high mobility group protein B1 through p38 mitogen-activated protein kinase pathway in

Ruike Wang1, Qinqin Zhang1, Shenghui Yang1

  • 1Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha 410008, China.

Abstract

Insights

Tumor necrosis factor-alpha (TNF-α) increases high mobility group protein B1 (HMGB1) in microglial cells via p38 MAPK. A p38 MAPK inhibitor, SB203580, suppressed this TNF-α-induced HMGB1 expression.

Area of Science:

  • Neuroinflammation
  • Cellular signaling pathways
  • Molecular biology

Background:

  • Microglial cells are key immune cells in the central nervous system.
  • High mobility group protein B1 (HMGB1) is implicated in inflammatory responses.
  • Tumor necrosis factor-alpha (TNF-α) is a pro-inflammatory cytokine.

Purpose of the Study:

  • To investigate the role of the p38 mitogen-activated protein kinase (MAPK) pathway in TNF-α-induced HMGB1 expression in microglial cells.
  • To evaluate the effect of the p38 MAPK inhibitor SB203580 on HMGB1 expression.

Main Methods:

  • Microglial cells were treated with TNF-α, SB203580, or both.
  • Protein levels of phosphorylated p38 MAPK (p-p38 MAPK) and HMGB1 were measured using ELISA and Western Blot.
  • HMGB1 mRNA levels were assessed via RT-PCR.

Main Results:

  • TNF-α significantly increased p-p38 MAPK and HMGB1 protein and mRNA levels in microglial cells.
  • Treatment with SB203580 effectively suppressed the TNF-α-induced upregulation of HMGB1 at both protein and mRNA levels.

Conclusions:

  • The p38 MAPK pathway is activated by TNF-α in microglial cells.
  • TNF-α upregulates HMGB1 expression in microglial cells through the activation of the p38 MAPK pathway.

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