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Regulation of the polymeric immunoglobulin receptor by water intake and vasopressin in the rat kidney.

机译:通过大鼠肾脏中的水分摄入和加压素调节聚合免疫球蛋白受体。

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摘要

The polymeric immunoglobulin receptor (pIgR) transports polymeric immunoglobulins (IgA) from the basolateral to the apical surface of epithelial cells. At the apical surface, its amino-terminal domain, termed secretory component (SC), is proteolytically cleaved and released either unbound (free SC) or bound to IgA. We examined the effects of changes in water balance and vasopressin on the production and secretion of the pIgR in the rat kidney in vivo. Water deprivation induced a 2.7-fold increase in the pIgR mRNA and a 2.2-fold increase in intracellular pIgR protein compared with water-loaded animals. Physiological doses of desmopressin reproduced the effects of water deprivation on mRNA and intracellular protein levels, suggesting that pIgR expression may be regulated by a vasopressin-coupled mechanism. Secretion of free SC and secretory IgA in the urine, however, correlated directly with water intake and urine flow. These results suggest that hydration status and vasopressin may affect the mucosal immunity of the kidney by regulating at different steps the epithelial cell production and secretion of the polymeric immunoglobulin transporter/ secretory component.
机译:聚合免疫球蛋白受体(pIgR)将聚合免疫球蛋白(IgA)从基底外侧转移到上皮细胞的顶表面。在其顶端表面,其氨基末端结构域(称为分泌成分(SC))被蛋白水解切割并释放出未结合的(游离SC)或结合到IgA。我们检查了体内大鼠体内水平衡和加压素的变化对pIgR产生和分泌的影响。与充满水的动物相比,缺水导致pIgR mRNA增加2.7倍,细胞内pIgR蛋白增加2.2倍。去氨加压素的生理剂量再现了水剥夺对mRNA和细胞内蛋白质水平的影响,表明pIgR表达可能受血管加压素偶联机制的调节。但是,尿液中游离SC和分泌型IgA的分泌与饮水量和尿液流量直接相关。这些结果表明水合状态和加压素可通过在不同步骤调节上皮细胞的产生和聚合免疫球蛋白转运蛋白/分泌成分的分泌来影响肾脏的粘膜免疫。

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