PMID- 17923043 OWN - NLM STAT- MEDLINE DCOM- 20081203 LR - 20181201 IS - 0376-2491 (Print) IS - 0376-2491 (Linking) VI - 87 IP - 28 DP - 2007 Jul 24 TI - [Protein kinase C-betaI, betaII in mouse diabetic nephropathy kidney and its relation to nephroprotective actions of the angiotensin receptor blocker telmisartan]. PG - 1991-5 AB - OBJECTIVE: To investigate the localization and expression of protein kinase C (PKC)-betaI, betaII in diabetic nephropathy (DN) mouse kidney and its relation to angiotensin receptor blocker telmisartan (Micardis). METHODS: Eighteen mice were divided into three groups: normal group, DN group and Micardis-treated group (n = 6, each group). The expression of PKC-betaI, betaII, transforming growth factor- beta 1 (TGF-beta1) and vascular endothelial growth factor (VEGF) in glomeruli was measured by semiquantitative immunofluorescence histochemistry, the localization of PKC-betaI, betaII was detected by confocal immunofluorescence laser scanning microscopy and the expression of PKC-betaI, betaII in renal cortex, outer and inner medulla were evaluated by semiquantitative Western blotting. RESULTS: Compared to normal mice, the expression of PKC-betaI and betaII on apical membrane of proximal tubule epithelial cells of DN mice was significantly increased, whereas the expression of PKC-betaII on cortical and inner medullary collecting duct was decreased. Western blotting detected increasing expression of PKC-betaI in the renal cortex and outer medulla (P < 0.01), and decreasing expression of PKC-betaII in renal cortex of DN mice (P < 0.01). Enhanced expression of PKC-betaI as well as TGF-beta1 and VEGF (P < 0.01) were shown in the glomeruli of DN mice, where the expression of PKC-betaII was decreased (P < 0.05). Meanwhile, PKC-betaI exhibited a positive correlation to TGF-beta1 (r = 0.649, P = 0.030), but no correlation to VEGF (r = 0.387, P = 0.079). Micardis could partly attenuate above changes. CONCLUSION: The localization and expression of PKC-betaI, betaII are altered in DN mice, PKC-betaI, betaII may change the function of proximal tubule and PKC-betaI may contribute to glomerular hypertrophy through influencing the expression of glomerular TGF-beta1. Treatment with Micardis can partly improve the abnormal expression and distribution of PKC-betaI, betaII in kidneys of DN mice, which suggests that renin-angiotensin-system is implicated in the pathogenesis of DN by regulating the expression and activation of PKC-betaI, betaII isoforms. FAU - Yao, Li-jun AU - Yao LJ AD - Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. FAU - Wang, Jian-qing AU - Wang JQ FAU - Deng, An-guo AU - Deng AG FAU - Liu, Jian-she AU - Liu JS LA - chi PT - Journal Article PL - China TA - Zhonghua Yi Xue Za Zhi JT - Zhonghua yi xue za zhi JID - 7511141 RN - 0 (Angiotensin II Type 1 Receptor Blockers) RN - 0 (Benzimidazoles) RN - 0 (Benzoates) RN - 0 (Isoenzymes) RN - 0 (Transforming Growth Factor beta1) RN - 0 (Vascular Endothelial Growth Factor A) RN - EC 2.7.11.13 (Protein Kinase C) RN - U5SYW473RQ (Telmisartan) SB - IM MH - Angiotensin II Type 1 Receptor Blockers/*pharmacology MH - Animals MH - Benzimidazoles/*pharmacology MH - Benzoates/*pharmacology MH - Diabetic Nephropathies/enzymology/pathology/*prevention & control MH - Fluorescent Antibody Technique MH - Isoenzymes/metabolism MH - Kidney/*drug effects/enzymology/pathology MH - Male MH - Mice MH - Mice, Inbred C57BL MH - Protein Kinase C/*metabolism MH - Telmisartan MH - Transforming Growth Factor beta1/metabolism MH - Vascular Endothelial Growth Factor A/metabolism EDAT- 2007/10/10 09:00 MHDA- 2008/12/17 09:00 CRDT- 2007/10/10 09:00 PHST- 2007/10/10 09:00 [pubmed] PHST- 2008/12/17 09:00 [medline] PHST- 2007/10/10 09:00 [entrez] PST - ppublish SO - Zhonghua Yi Xue Za Zhi. 2007 Jul 24;87(28):1991-5.