Interestingly, serum vitamin A was dependent on serum Vitamin B12

Interestingly, serum vitamin A was dependent on serum Vitamin B12. Immunohistochemistry showed that megalin and cubilin were accumulated at the apical surface of the proximal tubules in B12-Def., and restored in 24 hrs and 7days-CNB12. However megalin expression was not changed at protein and RNA level. Therefore, it is suggested that vitamin B12 deficiency

suppresses the endocytosis via megalin. As a result of confocal imaging, RBP reuptake-vesicles were decreased size and numbers in B12-Def. and restored in 7days-CNB12. RBP expression at protein level was dependent on serum Vitamin B12 level, whereas RBP mRNA was not changed. Conclusion: The www.selleckchem.com/products/byl719.html present data shows that vitamin B12 status is linked to endocytosis via megalin, and reabsorption of vitamin A in the kidney. EIAM-ONG SOMCHIT1, SINPHITUKKUL KITTISAK2, MANOTHAM KRISSANAPONG3, EIAM-ONG SOMCHAI4 1Chulalongkorn

University; 2Chulalongkorn University; 3Lerdsin Hospital; 4Chulalongkorn University Introduction: Previous in vitro study showed that aldosterone rapidly stimulates PKC alpha that could activate alpha1 isoform of Na, K-ATPase and then enhances its activity. There are no in vivo data demonstrating the rapid effects of aldosterone on renal protein expressions of PKC alpha and alpha1-Na, K-ATPase simultaneously. The present study further investigates the expression of these proteins. Methods: Male Wistar rats were intraperitoneally injected with normal saline solution or aldosterone (150 mg/kg BW). After 30 minutes, abundances FDA approved Drug Library and localizations of PKC alpha and alpha1-Na, K-ATPase proteins were determined by western blot analysis and immunohistochemistry, respectively. Results: Aldosterone administration significantly increased MG-132 concentration plasma aldosterone levels from 1,251.95 ± 13.83 to be 6,521.78 ± 209.92 pmol/L. By western blot analysis, aldosterone enhanced renal protein abundances of PKC alpha (tissue homogenate) and alpha1-Na, K-ATPase (plasma membrane) approximately 50% and 30%, respectively (P < 0.05). From immunohistochemistry examination in sham group, the protein

expression of PKC alpha was prominent in the medulla. Aldosterone stimulated the expression both in cortex and medulla with the translocation from basolateral to luminal side of proximal convoluted tubule. For alpha1-Na, K-ATPase protein expression, the sham rats showed a strong immunostaining in the distal convoluted tubule, collecting duct, and thick ascending limb. Aldosterone elevated the expression in the proximal convoluted tubule and medullary collecting duct. Conclusion: This in vivo study is the first to demonstrate simultaneously that aldosterone rapidly elevates PKC alpha and alpha1-Na, K-ATPase protein abundances in rat kidney. Both immunoreactivities were stimulated in cortex and medulla. The greater affected areas were noted for PKC alpha expression, whereas the alterations of alpha1-Na, K-ATPase were observed only in the proximal tubule and medullary collecting duct.

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