Summary
The expression of c-met stimulated by high glucose in human renal tubular epithelial cells and the role of HGF/c-met system in diabetic nephropathy were examined. The proximal tubular epithelial cells were cultured in vitro under different conditions. MTT was used for the detection of cellular proliferation and RT-PCR was employed for measurement of c-met mRNA level. Our results showed that under different conditions, there were no significant differences in the proliferation of proximal tubular epithelial cells 12 h and 24 h after the culuture (P>0.05). The proliferation of proximal tubular epithelial cells showed a significant change 96 h after the culture and the cellular proliferation induced by hepatocyte growth factor (HGF) was very active (P<0.05). Moreover, no significant difference in the expression of c-met mRNA was found 12 h after the culture under different conditions (P>0.05), while 24 and 96 h after the culture, a persistent and significantly higher expression of c-met mRNA was found in HGF-induced proliferation. It is concluded that addition of exogenous HGF could inhibit the apoptosis induced by high-level glucose, promote the proliferation of proximal tubular epithelial cells, and induce the expression of c-met. Our study suggests that local up-regulation of HGF/c-met system plays an important role in the repair of renal damage in diabetic nephropathy.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Matsumoto K, Nakamura T. Hepatocyte growth factor: renotropic role and potential therapeutics for renal disease. Kidney Int, 2001,59(5):2023–2038
Nakamura T, Nishizawa T, Hagiya M et al. Molecular cloning and expression of human hepatocyte growth factor. Nature, 1994,342(6248):440–443
Mizuno S, Matsumoto K, Kurosawa T et al. Reciprocal balance of hepatocyte growth factor and transforming growth factor-β 1 in renal fibrosis in mice. Kidney International, 2000,57(3):937–948
Wang S N, Lapage J, Hirschberg R. Role of glomerular ultrafiltration of growth factor in progressive interstitial fibrosis in diabetic nephropathy. Kidney Int, 2000,57(3):1002–1014
Wen X Y, Zhen F L. A preliminary study on the inhibitory effect of hepatocyte growth factor on the transdifferentiation of tubular epithelia. Chin J Intergr Tradit West Nephrol (Chinese), 2002,3(7):380–382
Mizuno S, Kurosawa T, Matsumoto K et al. Hepatocyte growth factor prevents renal fibrosis and dysfunction in a mouse model of chronic renal disease. J Clin Invest, 1998,101(9):1827–1834
Kobayashi E, Sasamura H, Mifune M et al. Hepatocyte growth factor regulates proteoglycan synthesis in interstitial fibroblasts. Kidney Int, 2003,64(4):1179–1188
Liu Y, Rajur K, Tolbert E et al. Endogenous hepatocyte growth factor ameliorates chronic renal injury by activating matrix degradation pathways. Kidney Int, 2000,58(5):2028–2043
Mou S, Zhang Q Y, Zhao H F et al. Expression of hepatocyte growth factor and c-met stimulated by high glucose in human kidney fibroblast and its significance. Chin J Endocrinol (Chinese), 2002,18(4):260–263
Cruzado J M, Lloheras N, Torras J et al. Regression of advanced diabetic nephropathy by hepatocyte growth factor gene therapy in rats. Diabetes, 2004,53(4):1119–1127
Dai C, Li Y, Yang J et al. Hepatocyte growth factor preserves beta cell mass and mitigates hyperlycemia in streptozotocin-induced diabetic mice. J Biol Chem, 2003,278(27):80–87
Author information
Authors and Affiliations
Additional information
LI Xing, male, born in 1961, Professor
Rights and permissions
About this article
Cite this article
Xing, L., Muxun, Z. Expression of c-met stimulated by high glucose in human renal tubular epithelial cells and its implication. J. Huazhong Univ. Sc. Technol. 27, 161–163 (2007). https://doi.org/10.1007/s11596-007-0213-z
Received:
Issue Date:
DOI: https://doi.org/10.1007/s11596-007-0213-z