Prostaglandin Synthesis and Inactivation in Kidneys …

Theseprostaglandins may exert important physiologic effects, because reninsecretion and arteriolar resistance are regulated by the glomerulus andthe afferent and efferent arterioles.

Regucalcin has been shown to exert suppressiveeffects on DNA synthesis activity in the nuclei isolated from ratrenal cortiex (). Such an effect was induced byadding of regucalcin (0.1-0.5 M) to the reaction mixture(). Also, the suppressiveeffects of regucalcin were noted in the presence of calciumchloride (50 M) in the reaction mixture, and thissuppression was potentiated in the presence of EGTA (1 mM)(). The suppressive effects ofregucalcin on nuclear DNA synthesis were thus mediated through amechanism unrelated to Ca. The presence ofanti-regucalcin monoclonal antibody (10-50 ng/ml) in the reactionmixture caused an increase in nuclear DNA synthesis activity(). This increase wascompletely abolished by the addition of exogenous regucalcin (0.5M) (). Regucalcin candirectly bind to nuclear DNA and inhibit DNA synthesis (). Nuclear regucalcin may play a rolein the suppression of nuclear DNA synthesis in kidney proximaltubular epithelial cells ().

Bardoxolone Methyl and Kidney Function in CKD with …

Regucalcin in the cytoplasm of kidney cells isdemonstrated to localize into the nucleus, and it has been found toregulate nuclear function; regucalcin was found to localize in thenucleus of HA-regucalcin/phCMV2-transfected NRK52E cells usingimmunocytochemical and western blot analysis (). The nuclear localization ofregucalcin was enhanced after culture with FBS, PTH, Bay K 8644 orPMA (). This enhancement wasremarkable following culture with PMA, which is an activator ofprotein kinase C, and it was suppressed by staurosporine, aninhibitor of protein kinase C (). Thus, the nuclear localization ofregucalcin was enhanced through Ca-signaling factorsincluding protein kinase C in NRK52E cells (). The stimulatory effect of PTH onregucalcin mRNA expression in NRK52E cells was mediated throughcAMP or IP-released Ca and protein kinaseC (). Thus, it has beendemonstrated that protein kinase C enhances both regucalcin mRNAexpression and nuclear localization of regucalcin protein in NRK52Ecells.

Endogenous regucalcin may suppress the activity ofvarious protein phosphatases in the kidney cortex cells. Of note,nuclear regucalcin was found to suppress calcineurin,serine/threonine phosphatase and tyrosine phosphatase that arepresent in the nucleus of rat kidney cortex cells (). The administration of calcium inrats was shown to increase the levels of regucalcin and cause acorresponding rise in protein phosphatase activity in the cytoplasmand nucleus of the kidney cortex (). The presence of anti-regucalcinmonoclonal antibody in the enzyme reaction mixture caused anincrease in protein phosphatase in the cytoplasm and nucleus ofnormal rat kidney cortex ().The increased levels of endogenous regucalcin were suggested tosuppress protein phosphatase activity enhanced in the cytoplasm andnucleus of the kidney cortex of calcium-administered rats. Thedephosphorylation of many phosphorylated proteins is regulated byprotein phosphatase, which is implicated in nuclear transcriptionalregulation in various cell types (). Thus, it is posited in this studythat regucalcin may play a role in the regulation of nuclearsignaling-related gene expression, through the inhibition ofnuclear protein phosphatase activity.

The blockade of prostaglandin synthesis with ..

Morooka Y and Yamaguchi M: Inhibitoryeffect of regucalcin on protein phosphatase activity in the nucleiof rat kidney cortex. J Cell Biochem. 83:111–120. 2001. : :

Xue JH, Takahashi H and Yamaguchi M:Stimulatory effect of regucalcin on mitochondrial ATP-dependentcalcium uptake activity in rat kidney cortex. J Cell Biochem.80:285–292. 2000. : :

Prostaglandin Synthesis - [PDF Document]

Regucalcin has been demonstrated to regulate thegene expression of various proteins related to mineral iontransport in kidney cells. To determine the role of endogenousregucalcin, NRK52E cells (transfectants) overexpressing regucalcinwere generated in a previous study (). In regucalcin/pCXN2-transfectedcells regucalcin overexpression was increased 21-fold as comparedwith that of the parental wild-type NRK52E cells (). The overexpression of endogenousregucalcin was found to increase rat outer medullary Kchannel (ROMK) mRNA expression in NRK52E cells, although it did notalter the expression of type II NaPi cotransporter (NaPi-IIa),Na, K-ATPase, epithelial sodium channel(ENaC) or angiotensinogen mRNAs (). Culture with aldosterone caused anincrease in ENaC, Na, K-ATPase and ROMKmRNA expression in wild-type NRK52E cells (). The effect of aldosterone inincreasing ENaC and Na, K-ATPase mRNAexpression was not observed in the transfectants (). Aldosterone was shown to upregulateregucalcin mRNA expression in NRK52E cells (). The stimulatory effect ofaldosterone on ENaC and Na, K-ATPase mRNAexpressions may thus be partly mediated through endogenousregucalcin in NRK52E cells.

prostaglandin synthesis in the Goldblatt hypertensive rat

In all groups of animals, the nonselective COX inhibitors induced an increase in renal vascular resistance and a consequent decrease in glomerular filtration rate and renal blood flow.

Prostaglandin Kidney - Prostaglandin Questions

This observation illustrates the major renal protective role played by the vasodilatory prostaglandins during the neonatal period, when the kidney is perfused at very low perfusion pressure.

Renal Prostaglandin Synthesis - Prostaglandin Quizlet

The overexpression of endogenous regucalcin wasfound to exert suppressive effects on the mRNA expression of theL-type Ca channel and calcium-sensing receptor (CaR),which regulate intracellular Ca signaling and renalCa transport in NRK52E cells (,). The entry of Cathrough L-type Ca channels induces mitochondrialdisruption and cell death ().The blockade of Ca influx through L-typeCa channels has been shown to attenuate mitochondrialinjury and apoptosis in hypoxia of renal tubular cells (). Regucalcin may regulate theintracellular Ca signaling pathway, which is mediatedthrough its suppressive effect on L-type Ca channel orCaR mRNA expressions in the kidney proximal tubular epithelialcells.