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

1998 ◽  
Vol 101 (9) ◽  
pp. 1827-1834 ◽  
Author(s):  
S Mizuno ◽  
T Kurosawa ◽  
K Matsumoto ◽  
Y Mizuno-Horikawa ◽  
M Okamoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Renal Disease ◽  
Hepatocyte Growth Factor ◽  
Renal Fibrosis ◽  
Chronic Renal Disease ◽  
Hepatocyte Growth

Serum hepatocyte growth factor levels in patients with chronic renal disease - effect of GFR and pathogenesis

2001 ◽  
Vol 61 (8) ◽  
pp. 615-619 ◽  
Author(s):  
E. Randers ◽  
E. J. Erlandsen ◽  
J. H. Kristensen ◽  
S. Markussen ◽  
O. L. Pedersen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Disease ◽  
Hepatocyte Growth Factor ◽  
Chronic Renal Disease ◽  
Disease Effect ◽  
Hepatocyte Growth

Hepatocyte growth factor predicts survival and relates to inflammation and intima media thickness in end-stage renal disease

2000 ◽  
Vol 36 (5) ◽  
pp. 945-952 ◽  
Author(s):  
Lorenzo S. Malatino ◽  
Francesca Mallamaci ◽  
Francesco A. Benedetto ◽  
Ignazio Bellanuova ◽  
Alessandro Cataliotti ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Disease ◽  
Hepatocyte Growth Factor ◽  
End Stage Renal Disease ◽  
Intima Media Thickness ◽  
Media Thickness ◽  
Stage Renal Disease ◽  
End Stage ◽  
Hepatocyte Growth

Hepatocyte growth factor overexpression ameliorates liver inflammation and fibrosis in a mouse model of nonalcoholic steatohepatitis

2011 ◽  
Vol 6 (3) ◽  
pp. 620-630 ◽  
Author(s):  
Hiroki Tojima ◽  
Satoru Kakizaki ◽  
Takashi Kosone ◽  
Norio Horiguchi ◽  
Yuichi Yamazaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Hepatocyte Growth Factor ◽  
Nonalcoholic Steatohepatitis ◽  
Liver Inflammation ◽  
Hepatocyte Growth

scholarly journals Actions of hepatocyte growth factor as a local modulator in the kidney: Potential role in pathogenesis of renal disease

1998 ◽  
Vol 53 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Yoshikage Yo ◽  
Ryuichi Morishita ◽  
Kei Yamamoto ◽  
Naruya Tomita ◽  
Iwao Kida ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Disease ◽  
Hepatocyte Growth Factor ◽  
Potential Role ◽  
Hepatocyte Growth

Abstract 1494: Hepatocyte Growth Factor Attenuates Angiotensin II Induced Renal Fibrosis through TGF-β1 Suppression by Anoikis of Myofibroblasts

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kazuma Iekushi ◽  
Yoshiaki Taniyama ◽  
Junya Azuma ◽  
Fumihiro Sanada ◽  
Norio Dosaka ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Renal Fibrosis ◽  
Type I ◽  
Ang Ii ◽  
Wild Type ◽  
Induced Apoptosis ◽  
Hepatocyte Growth ◽  
Tgf Β1

Progression of chronic kidney disease (CKD) is characterized by the persistent accumulation of extracellular matrix. Especially, α-SMA positive myofibroblast which produce high amounts of TGF-β1 are considered to play a key role in interstitial fibrosis. Previous studies demonstrated that hepatocyte growth factor (HGF) improved kidney fibrosis in murine models, where direct molecular mechanisms of myofibroblasts have not yet been understood. We tested the hypothesis in vivo using cardiac specific overexpression HGF mice (HGF-Tg), which showed a significant increase in serum HGF concentration. Angiotensin II (Ang II) infusion significantly induced renal fibrosis in wild type mice, while renal fibrosis was significantly decreased in HGF-Tg mice accompanied by the degrease in interstitial myofibroblasts (P<0.05). Quantitative analysis demonstrated 1.69-folds induction of profibrtic cytokine, TGF-β1 mRNA in HGF-Tg with Ang II group compared with wild type with Ang II, and Collagen type I and IV mRNA expression was significantly decreased in HGF-Tg mice with Ang II. The antifibotic action of HGF-Tg mice was concordant with an increase in MMP-2, MMP-9 expression (1.32-fold, 1.33-fold vs wild type with Ang II infusion, P<0.05, respectively), and decreased TIMP-1, TIMP-2 expression (1.5-fold, 1.28-fold vs wild type with Ang II infusion, P<0.05, respectively). To further investigate the anti-fibrotic effect of HGF, we used cultured human mesangial cells (HMC). When HMC were treated with TGF-β1, cells underwent to phenotypic change similar to myofibroblasts, accompanied by the significant increase in c-Met/HGF receptor (P<0.05). Under such conditions, HGF induced anoikis-induced apoptosis of myofibroblasts. It also linked with FAK phosphorylation especially p-FAK (Y925) (P<0.05). When GM6001 (a broad-spectrum MMP inhibitor) was added with HGF, HGF-induced apptosis was significantly decreased. It was suggested that increased activities of MMPs underlie the major mechanism of HGF mediated anoikis induced apoptosis. The present study demonstrated that HGF elicited myofibroblast anoikis. Activation of MMPs in fibrotic kidney might be considered as a target to attenuate the progression of CKD.

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