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Research Article Free access | 10.1172/JCI1709

Hepatocyte growth factor prevents renal fibrosis and dysfunction in a mouse model of chronic renal disease.

S Mizuno, T Kurosawa, K Matsumoto, Y Mizuno-Horikawa, M Okamoto, and T Nakamura

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Mizuno, S. in: JCI | PubMed | Google Scholar

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Kurosawa, T. in: JCI | PubMed | Google Scholar

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Matsumoto, K. in: JCI | PubMed | Google Scholar

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Mizuno-Horikawa, Y. in: JCI | PubMed | Google Scholar

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Okamoto, M. in: JCI | PubMed | Google Scholar

The Institute of Experimental Animal Sciences, Department of Oncology, Biomedical Research Center, Osaka University Medical School, Suita 565-0871, Japan.

Find articles by Nakamura, T. in: JCI | PubMed | Google Scholar

Published May 1, 1998 - More info

Published in Volume 101, Issue 9 on May 1, 1998
J Clin Invest. 1998;101(9):1827–1834. https://doi.org/10.1172/JCI1709.
© 1998 The American Society for Clinical Investigation
Published May 1, 1998 - Version history
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Abstract

Chronic renal disease (CRD) is generally thought to be incurable, except through renal transplantation, and the number of patients with CRD is on the increase. Glomerulosclerosis and tubulointerstitial fibrosis represent the morphological equivalent of end-stage CRD. In this study, we demonstrated the preventive effect of hepatocyte growth factor (HGF) on the progression of renal dysfunction and fibrosis, using a spontaneous mouse model for CRD (ICGN strain). The mice progressively developed glomerular sclerotic injury, tubular atrophy, and renal dysfunction until they were 17 wk of age. When recombinant HGF was injected into these mice during a 4-wk-period (from weeks 14-17 after birth), DNA synthesis of tubular epithelial cells was found to be 4.4-fold higher than in mice without HGF injection, thereby suggesting tubular parenchymal expansion promoted by HGF. Notably, HGF suppressed the expression of transforming growth factor-beta and of platelet-derived growth factor as well as myofibroblast formation in the affected kidney. Consequently, the onset of tubulointerstitial fibrosis was almost completely inhibited by HGF, while HGF attenuated the progression of glomerulosclerosis, both leading to preventing manifestation of renal dysfunction. From our results, supplement therapy with HGF may be taken into consideration as a novel option for prevention and treatment of CRD.

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