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首页> 外文期刊>American Journal of Physiology >Physiological regulation of cyclooxygenase-2 in the kidney.
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Physiological regulation of cyclooxygenase-2 in the kidney.

机译：肾脏中环氧合酶2的生理调节。

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In adult mammalian kidney, cyclooxygenase-2 (COX-2) expression is found in a restricted subpopulation of cells. The two sites of renal COX-2 localization detected in all species to date are the macula densa (MD) and associated cortical thick ascending limb (cTALH) and medullary interstitial cells (MICs). Physiological regulation of COX-2 in these cellular compartments suggests functional roles for eicosanoid products of the enzyme. COX-2 expression increases in high-renin states (salt restriction, angiotensin-converting enzyme inhibition, renovascular hypertension), and selective COX-2 inhibitors significantly decrease plasma renin levels, renal renin activity, and mRNA expression. There is evidence for negative regulation of MD/cTALH COX-2 by angiotensin II and by glucocorticoids and mineralocorticoids. Conversely, nitric oxide generated by neuronal nitric oxide synthase is a positive modulator of COX-2 expression. Decreased extracellular chloride increases COX-2 expression in cultured cTALH, an effect mediated by increased p38 mitogen-activated protein kinase activity, and, in vivo, a sodium-deficient diet increases expression of activated p38 in MD/cTALH. In contrast to COX-2 in MD/cTALH, COX-2 expression increases in MICs in response to a high-salt diet as well as water deprivation. Studies in cultured MICs have confirmed that expression is increased in response to hypertonicity and is mediated, at least in part, by nuclear factor-kappaB activation. COX-2 inhibition leads to apoptosis of MICs in response to hypertonicity in vitro and after water deprivation in vivo. In addition, COX-2 metabolites appear to be important mediators of medullary blood flow and renal salt handling. Therefore, there is increasing evidence that COX-2 is an important physiological mediator of kidney function.
机译：在成年哺乳动物的肾脏中，在细胞的受限制亚群中发现了环氧合酶2（COX-2）的表达。迄今为止，在所有物种中检测到的肾脏COX-2定位的两个位点是黄斑窝（MD）以及相关的皮质厚上升肢（cTALH）和髓质间质细胞（MIC）。在这些细胞区室中，COX-2的生理调节表明该酶的类花生酸产物具有功能性作用。在高肾素状态（盐限制，血管紧张素转换酶抑制，肾血管性高血压）中，COX-2表达增加，而选择性COX-2抑制剂可显着降低血浆肾素水平，肾素活性和mRNA表达。有证据表明血管紧张素II以及糖皮质激素和盐皮质激素对MD / cTALH COX-2负调节。相反，神经元一氧化氮合酶产生的一氧化氮是COX-2表达的正调节剂。减少的细胞外氯化物会增加培养的cTALH中COX-2的表达，这是由增加的p38丝裂原激活的蛋白激酶活性介导的，而在体内，缺钠饮食会增加MD / cTALH中激活的p38的表达。与MD / cTALH中的COX-2相比，MICs对高盐饮食和缺水的反应增加。在培养的MICs中的研究已经证实，表达在高渗反应中增加，并且至少部分地由核因子-κB激活介导。在体外和体内缺水后，COX-2抑制作用导致高渗性导致MICs凋亡。此外，COX-2代谢产物似乎是髓质血流和肾盐处理的重要介质。因此，越来越多的证据表明COX-2是肾脏功能的重要生理介质。

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