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首页> 外文期刊>American Journal of Physiology >PPAR-gamma inhibits ANG II-induced cell growth via SHIP2 and 4E-BP1.
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PPAR-gamma inhibits ANG II-induced cell growth via SHIP2 and 4E-BP1.

机译：PPAR-γ通过SHIP2和4E-BP1抑制ANG II诱导的细胞生长。

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摘要

The present study evaluated the effects of peroxisome proliferator-activated receptor (PPAR)-gamma activators on ANG II-induced signaling pathways and cell growth. Vascular smooth muscle cells (VSMC) derived from rat mesenteric arteries were treated with ANG II, with/without the AT1 receptor blocker valsartan or the AT2 receptor blocker PD-123319, after pretreatment for 24 h with the PPAR-gamma activators 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2) or rosiglitazone. Both 15d-PGJ2 and rosiglitazone decreased ANG II-induced DNA synthesis. Rosiglitazone treatment increased nuclear PPAR-gamma expression and activity in VSMC. However, rosiglitazone did not alter expression of PPAR-alpha/beta, ERK 1/2, Akt, or ANG II receptors. 15d-PGJ2 and rosiglitazone decreased ERK 1/2 and Akt peak activity, both of which were induced by ANG II via the AT1 receptor. Rosiglitazone inhibited ANG II-enhanced phosphorylation of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), as well as Src homology (SH) 2-containing inositol phosphatase 2 (SHIP2). PPAR-gamma activation reduced ANG II-induced growth associated with inhibition of ERK 1/2, Akt, 4E-BP1, and SHIP2. Modulation of these pathways by PPAR-gamma activators may contribute to regression of vascular remodeling in hypertension.
机译：本研究评估了过氧化物酶体增殖物激活受体（PPAR）-γ激活剂对ANG II诱导的信号通路和细胞生长的影响。在用PPAR-γ激活剂15-脱氧剂预处理24小时后，使用有/无AT1受体阻断剂缬沙坦或AT2受体阻断剂PD-123319的ANG II处理源自大鼠肠系膜动脉的血管平滑肌细胞（VSMC）。 δ（12,14）-前列腺素J2（15d-PGJ2）或罗格列酮。 15d-PGJ2和罗格列酮均降低了ANG II诱导的DNA合成。罗格列酮治疗可增加VSMC中核PPAR-γ的表达和活性。但是，罗格列酮不会改变PPAR-α/β，ERK 1/2，Akt或ANG II受体的表达。 15d-PGJ2和罗格列酮降低了ERK 1/2和Akt峰活性，两者均由ANG II通过AT1受体诱导。罗格列酮抑制ANG II增强的真核起始因子4E结合蛋白1（4E-BP1）磷酸化，以及Src同源（SH）2含肌醇磷酸酶2（SHIP2）。 PPARγ激活减少与抑制ERK 1/2，Akt，4E-BP1和SHIP2相关的ANG II诱导的生长。 PPAR-γ激活剂对这些途径的调节可能有助于高血压中血管重构的消退。

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