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首页> 外文期刊>Journal of Cellular Physiology >15-deoxy-delta 12,14-prostaglandin J(2) inhibits the synthesis of the acute phase protein SIP24 in cartilage: Involvement of COX-2 in resolution of inflammation.
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15-deoxy-delta 12,14-prostaglandin J(2) inhibits the synthesis of the acute phase protein SIP24 in cartilage: Involvement of COX-2 in resolution of inflammation.

机译：15-deoxy-delta 12日14-prostaglandin J(2)抑制急性期蛋白的合成SIP24软骨:cox - 2参与解决炎症。

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We previously demonstrated that, in the MC615 cartilage cell line, the p38/NF-kB pathway is activated both during differentiation and in response to an inflammatory stimulus. In both cases, the p38/NF-kB pathway activation leads to the expression of the lipocalin SIP24 and of COX-2. Given the fact that, in the same cells, the COX-2 expression is sustained during the inflammation resolution, at the same time that the SIP24 expression is suppressed, in the present study we tested the hypothesis that COX-2 products play a role in SIP24 repression. Taken together, our results suggest that, during the resolution of inflammation, COX-2 represses the acute phase protein SIP24 and restores physiological conditions, possibly through a pathway involving PPARgamma. Experimental evidences being the following: (1) 15-deoxy-delta 12,14-prostaglandin J(2), but not PGE(2): (i) inhibits the expression of SIP24 in the inflammatory phase and induces COX-2 synthesis; (ii) represses NF-kB activation induced by LPS; (iii) represses the synthesis of microsomal PGE Synthase-1 induced by LPS. (2) PPARgamma and PPARalpha are present in MC615 cells in both proliferating and hyperconfluent cultures. (3) PPARgamma ligand GW7845, but not PPARalpha ligand GW7647: (i) represses the expression of SIP24 induced by LPS; (ii) induces COX-2 expression. (4) p38 is involved in the PPARgamma mediated induction of COX-2. In fact 15-deoxy-delta 12,14-prostaglandin J(2) activates p38 and the cell pretreatment with the p38 specific inhibitor SB203580 represses the expression of COX-2 induced by both the 15-deoxy-delta12,14-prostaglandin J(2) and the PPARgamma ligand GW7845.
机译：我们先前表明,MC615软骨细胞系,p38 / NF-kB通路在分化和激活炎症反应刺激。情况下,p38 / NF-kB通路激活导致的表达lipocalin SIP24和的cox - 2。cox - 2表达持续期间炎症的决议,在同一时间SIP24表达抑制,本研究我们测试了cox - 2的假设产品在SIP24镇压中发挥作用。在一起,我们的研究结果表明,在解决炎症,cox - 2压制急性期蛋白SIP24和恢复生理条件下,可能通过涉及PPARgamma的途径。证据如下:(1)15-deoxy-delta12日,14-prostaglandin J(2),但不是铂族元素(2):(i)抑制SIP24的表达式炎症阶段和诱发cox - 2的合成;(2)压制NF-kB LPS引起的激活;(3)压制微粒体的合成铂族元素Synthase-1 LPS引起的。PPARalpha MC615细胞都存在增殖和hyperconfluent文化。PPARgamma配体GW7845,但不是PPARalpha配体GW7647:(我)压制SIP24的表达由有限合伙人;(4) p38是参与PPARgamma介导cox - 2的感应。12日,14-prostaglandin J(2)激活p38和细胞与p38特定抑制剂预处理SB203580压制cox - 2的表达诱导的15-deoxy-delta12 14-prostaglandin J(2)和PPARgamma ligand GW7845。

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