Summary
In current study, the expressions of protein kinase C (PKC)-α, βI and βII as well as their correlation to the expression of transforming growth factor-βI (TGF-βI) and vascular endothelial growth factor (VEGF) were investigated in glomeruli of normal renal tissues taken from human kidney tumors and kidney tissues from patients with diabetic nephropathy (DN). The accumulation of glomerular extracelluar matrix (ECM) was determined by PAS staining, the expressions of PKC-α, PKC-βI, PKC-βII, TGF-βI and VEGF were measured by semi-quantitative immunohistochemistry. Our results showed that in glomeruli of normal renal tissues, PKC-α and βII had a strong expression whereas the expression of PKC-βI was weak; in glomeruli of DN patients, the expressions of PKC-α, PKC-βI, VEGF and TGF-βI and the accumulation of ECM increased significantly, but the expression of PKC-βII decreased markedly. Meanwhile, the expressions of PKC-α and βI had a positive correlation to the expressions of VEGF and TGF-βI respectively, whereas PKC-βII showed no correlation to VEGF and TGF-βI. It is concluded that the expressions of PKC-α, βI and βII in glomeruli of normal subjects and DN patients are different. PKC-α seems to play a critical role in human DN by up-regulating VEGF expression, whereas PKC-βI is relatively important for the up-regulation of TGF-βI and the accumulation of ECM under diabetic conditions.
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References
Murphy M, McGinty A, Godson C. Protein kinase C: potential targets for intervention in diabetic nephropathy. Curr Opin Nephrol Hypertens, 1998,7:563–570
Cha D R, Kim N H, Yoon J W et al. Role of vascular endothelial growth factor in diabetic nephropathy. Kidney Int Suppl, 2000,77:S104–S112
Sharma K, Jin Y, Guo J et al. Neutralization of TGF-beta by anti-TGF beta antibody attenuates kidney hypertrophy and the enhanced extracellular matrix gene expression in STZ-induced diabetic mice. Diabetes, 1996,45(4):522–530
Redling S, Pfaff I L, Leitges M et al. Immunolocalization of protein kinase C isoenzymes α, βI, βII, δ, and ε in mouse kidney. Am J Physiol Renal Physiol, 2004,287(2):289–298
Pfaff I L, Wang H J, Volker V et al. Immunolocalization of Protein Kinase C Isoenzymes α, β I and β II in Rat Kidney. J Am Soc Nephrol, 1999,10(9):1861–1873
Kang N, Alexander G, Park J K et al. Differential expression of protein kinase C isoforms in streptozotocin-induced diabetic rats. Kidney Int, 1999,56:1737–1750
Ishii H, Jirousek M R, Koya D et al. Amelioration of vascular dysfunctions in diabetic rats by an oral PKC beta inhibitor. Science, 1996,272(5262):728–31
Menne J, Park J K, Boehne M et al. Diminished loss of proteoglycans and lack of albuminuria in protein kinase C-alpha-deficient diabetic mice. Diabetes, 2004,53(8):2101–2109
Kang D H, Hughes J, Mazzali M et al. Impaired angiogenesis in the remnant kidney model. II. Vascular endothelial growth factor administration reduces renal fibrosis and stabilizes renal function. J Am Soc Nephrol, 2001,12:1448–1457
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Yao, L., Wang, J., Mao, Y. et al. Different expressions of protein kinase C-α, βI and βII in glomeruli of diabetic nephropathy patients. J. Huazhong Univ. Sc. Technol. 26, 651–653 (2006). https://doi.org/10.1007/s11596-006-0605-5
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DOI: https://doi.org/10.1007/s11596-006-0605-5