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[Inhibitory effect of caveolin-1 on endoplasmic reticulum stress-induced apoptosis in macrophages via p38 MAPK

Wen Yue1, Shu-Tong Yao, Xiao Zhou

  • 1Pathophysiology Department, Taishan Medical College, Taian, China.

Sheng Li Xue Bao : [Acta Physiologica Sinica]
|April 20, 2012
PubMed

Insights

Caveolin-1 (Cav-1) suppresses endoplasmic reticulum (ER) stress-induced macrophage apoptosis by activating the p38 MAPK pathway. This finding is crucial for understanding atherosclerosis progression and potential therapeutic targets.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pathology

Context:

  • Endoplasmic reticulum (ER) stress is implicated in macrophage apoptosis within atherosclerotic lesions, contributing to plaque necrosis.
  • Caveolin-1 (Cav-1) is a protein involved in cellular signaling and membrane dynamics.

Purpose:

  • To investigate the role of Cav-1 in ER stress-induced apoptosis in cultured macrophages.
  • To elucidate the underlying molecular mechanisms involving p38 MAPK and CHOP.

Summary:

  • Thapsigargin (TG) treatment increased Cav-1 expression in RAW264.7 macrophages, which was dependent on caveolae and inhibited by filipin(III).
  • Inhibition of caveolae augmented TG-induced apoptosis and suppressed p38 MAPK phosphorylation, while CHOP expression remained unaffected.
  • Cav-1 appears to suppress ER stress-induced macrophage apoptosis via the p38 MAPK prosurvival pathway.

Impact:

  • Provides insights into the protective role of Cav-1 against ER stress in macrophages.
  • Identifies a potential mechanism linking Cav-1, ER stress, and macrophage survival in atherosclerosis.
  • Suggests Cav-1 and the p38 MAPK pathway as potential therapeutic targets for atherosclerosis.

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