Intracellular calcium signaling regulates glomerular filtration barrier permeability: the role of the PKGIα-dependent pathway

被引：14
|
作者：
Piwkowska, Agnieszka [1 ]
Rogacka, Dorota [1 ]
Audzeyenka, Irena [1 ]
Kasztan, Malgorzata [2 ]
Angielski, Stefan [1 ]
Jankowski, Maciej [1 ,3 ]
机构：
[1] Polish Acad Sci, Mossakowski Med Res Ctr, Lab Mol & Cellular Nephrol, Debinki 7, PL-80211 Gdansk, Poland
[2] Univ Alabama Birmingham, Dept Med, Cardiorenal Physiol & Med, Birmingham, AL 35294 USA
[3] Med Univ Gdansk, Dept Clin Chem, Gdansk, Poland
来源：
FEBS LETTERS | 2016年 / 590卷 / 12期
关键词：
calcium; contraction apparatus; Insulin; filtration barrier permeability; podocyte; CULTURED RAT PODOCYTES; SMOOTH-MUSCLE; SUBUNITS; CA2+; DIMERIZATION; ISOFORMS; KIDNEY; PUMP;
D O I：
10.1002/1873-3468.12228
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Podocytes are dynamic polarized cells that lie on the surface of glomerular capillaries and comprise an essential component of the glomerular filtration barrier. Insulin provoked a sustained, approximately 70%, increase in intracellular calcium concentration in podocytes. RT-PCR revealed the presence of mRNA encoding sarco/endoplasmic reticulum calcium ATPase isoforms 1-3, and plasma membrane Ca2+ pump (PMCA) isoforms 1,3,4; mRNA levels were depressed by the addition of insulin. Inhibitors of PMCA, and the Na+-Ca2+ exchanger, increased podocyte permeability to albumin, induced dimerization of protein kinase G type I alpha (PKGI alpha), and activation of PKGI alpha-dependent signaling. These data suggest the involvement of calcium and PKGI alpha signaling in insulin-enhanced filtration barrier permeability in podocytes.
引用
收藏
页码：1739 / 1748
页数：10
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