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首页> 外文期刊>American Journal of Physiology >Loss of prostaglandin E_2 release from immortalized urothelial cells obtained from interstitial cystitis patient bladders
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Loss of prostaglandin E_2 release from immortalized urothelial cells obtained from interstitial cystitis patient bladders

机译：从间质性膀胱炎患者膀胱获得的永生化尿道上皮细胞释放前列腺素E_2的损失

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摘要

Interstitial cystitis (IC) is associated with increased activated mast cell numbers in the bladder and impairment of the barrier function of the urothelium. We stimulated immortalized urothelial cells derived from the inflamed region of IC bladders (SR22A or SM28 abn) or from healthy bladders (PD07i or PD08i) with tryptase and measured phospholipase A_2 (PLA_2) activity and the resultant release of arachidonic acid and prostaglandin E_2 (PGE_2). Tryptase stimulation of either PD07i or SR22A resulted in similar increases in PLA_2 activity and arachidonic acid release. However, tryptase stimulation of SR22A and SM28 abn did not result in a significant increase in PGE_2 release compared with the increase in PGE_2 release from tryptase-stimulated PD07i and PD08i cells. Expression of mRNA for cyclooxygenase-2 and PGE synthase was lower and mRNA for 15-hydroxyprostaglandin dehydrogenase was higher in SR22A compared with PD07i, suggesting that both decreased synthesis and increased metabolism are responsible for the lack of a PGE_2 response in tryptase-stimulated SR22A cells. Since PGE_2 is a cytoprotective eicosanoid, the failure to produce this metabolite in cells isolated from the IC bladder may represent an increased susceptibility to damage by proinfammatory stimuli.
机译：间质性膀胱炎（IC）与膀胱中激活的肥大细胞数量增加和尿路上皮的屏障功能受损有关。我们用胰蛋白酶刺激了来自IC膀胱发炎区域（SR22A或SM28 abn）或健康膀胱（PD07i或PD08i）的永生化尿路上皮细胞，并测量了磷脂酶A_2（PLA_2）的活性以及由此产生的花生四烯酸和前列腺素E_2（PGE_2 ）。胰蛋白酶对PD07i或SR22A的刺激导致PLA_2活性和花生四烯酸释放的相似增加。然而，与受胰蛋白酶刺激的PD07i和PD08i细胞的PGE_2释放的增加相比，对SR22A和SM28 abn的胰蛋白酶的刺激并未导致PGE_2释放的显着增加。与PD07i相比，SR22A中环氧合酶2和PGE合酶的mRNA表达较低，而15-羟前列腺素脱氢酶的mRNA则较高，这表明在受胰蛋白酶刺激的SR22A细胞中，合成减少和代谢增加均导致缺乏PGE_2反应。由于PGE_2是一种具有细胞保护作用的类花生酸，因此无法在从IC膀胱分离出的细胞中产生这种代谢产物，这可能表示对原发性刺激的损害敏感性更高。

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