Rosiglitazone regulates anti-inflammation and growth inhibition via PTEN

Chiou Feng Lin, Kung Chia Young, Chyi Huey Bai, Bu Chin Yu, Ching Ting Ma, Yu Chieh Chien, Chiu Ling Chiang, Chao Sheng Liao, Hsin Wen Lai, Chiung Wen Tsao

研究成果: 雜誌貢獻文章同行評審

26 引文 斯高帕斯(Scopus)

摘要

Peroxisome proliferator-activated receptor gamma (PPAR γ) agonist has anti-inflammatory and anticancer properties. However, the mechanisms by which PPAR γ agonist rosiglitazone interferes with inflammation and cancer via phosphatase and tensin homolog-(PTEN)-dependent pathway remain unclear. We found that lower doses (2) production (via cyclooxygenase-2, COX-2), and activation of Akt in RAW 264.7 murine macrophages. However, rosiglitazone did not inhibit the production of reactive oxygen species (ROS). In PTEN knockdown (shPTEN) cells exposed to LPS, rosiglitazone did not inhibit NO release, PGE2 production, and activation of Akt. These cells had elevated basal levels of iNOS, COX-2, and ROS. However, higher doses (25-100 M) of rosiglitazone, without LPS stimulation, did not block NO release and PGE2 productions, but they inhibited p38 MAPK phosphorylation and blocked ROS generation in shPTEN cells. In addition, rosiglitazone caused G1 arrest and reduced the number of cells in S + G2/M phase, leading to growth inhibition. These results indicate that the anti-inflammatory property of rosiglitazone is related to regulation of PTEN independent of inhibition on ROS production. However, rosiglitazone affected the dependence of PTEN-deficient cell growth on ROS.

原文英語
文章編號787924
期刊BioMed Research International
2014
DOIs
出版狀態已發佈 - 2014
對外發佈

ASJC Scopus subject areas

  • 生物化學、遺傳與分子生物學 (全部)
  • 免疫學與微生物學 (全部)
  • 醫藥 (全部)

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