p38 MAPK might be at play as a pivotal intracellular signal transducer in endometriosis

Osamu Yoshino, Yutaka Osuga, Tetsu Yano, Osamu Tsutsumi, Yuji Taketani
In: Ensho Saisei · 2004 · vol. 24(6) , pp. 629–633 · doi:10.2492/jsir.24.629 · W2035973029
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Inhibition of p38 MAPK with FR 167653 reduced endometriotic lesion growth and intraperitoneal inflammation in a mouse model.

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This paper is a mini-review and accompanying experimental study assessing whether MAPK-driven inflammatory signaling is involved in endometriosis, focusing on p38MAPK as a potential intracellular signal transducer. In vitro, MAPK inhibitors tested suppressed IL-1β–induced IL-6 and IL-8 secretion and IL-1β–induced COX-2 expression in endometriotic cells, with the p38MAPK inhibitor FR 167653 showing the strongest inflammatory blockade. In an experimental mouse model, FR 167653 reduced the growth of endometriotic lesions and suppressed intraperitoneal inflammation, although the key limitation is that the evidence is presented from inhibitor-focused experiments rather than broader mechanistic validation. This paper is centrally about endometriosis — it argues for a p38MAPK-mediated inflammatory pathway and evaluates FR 167653’s effects in vitro and in mice.

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Abstract

Given the current theory of inflammatory changes being involved in the progression of endometriosis, MAPKs might be at play as pivotal intracellular signal transducers in endometriotic cells and thus have a pathophysiological role in the disease. In vitro study using endometriotic cell, all the MAPK inhibitors examined suppressed IL-1β-induced secretion of IL-6 and IL-8, and IL-1β-induced expression of COX-2 in endometriotic cells. Among MAPK inhibitors, p38MAPK inhibitor seemed to have the best potential to block inflammation. Then, the authors evaluated the effect of FR 167653, a p38MAPK inhibitor, on the development of endometriotic lesions and on the intraperitoneal inflammatory status using experimental model mice for endometriosis. FR 167653, a p38 MAPK inhibitor, caused a reduction in the growth of endometriotic lesions, coupled with the suppression of intraperitoneal inflammation. Thus, p38 MAPK inhibitors could have the therapeutic potential for endometriosis.
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Mini Review 子宮内膜症におけるMAPKを介する炎症の解析と新たな治療戦略 2004 年 24 巻 6 号 p. 629-633 詳細 抄録 Given the current theory of inflammatory changes being involved in the progression of endometriosis, MAPKs might be at play as pivotal intracellular signal transducers in endometriotic cells and thus have a pathophysiological role in the disease. In vitro study using endometriotic cell, all the MAPK inhibitors examined suppressed IL-1β-induced secretion of IL-6 and IL-8, and IL-1β-induced expression of COX-2 in endometriotic cells. Among MAPK inhibitors, p38MAPK inhibitor seemed to have the best potential to block inflammation. Then, the authors evaluated the effect of FR 167653, a p38MAPK inhibitor, on the development of endometriotic lesions and on the intraperitoneal inflammatory status using experimental model mice for endometriosis. FR 167653, a p38 MAPK inhibitor, caused a reduction in the growth of endometriotic lesions, coupled with the suppression of intraperitoneal inflammation. Thus, p38 MAPK inhibitors could have the therapeutic potential for endometriosis. © 2004 日本炎症･再生医学会

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endometriosis

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