A possible mechanism for prevention of intestinal programmed cell death after ischemia-reperfusion injury by hepatocyte growth factor pretreatment

2002 ◽  
Vol 37 (12) ◽  
pp. 1696-1699 ◽  
Author(s):  
Keith A. Kuenzler ◽  
L.Grier Arthur ◽  
Marshall Z. Schwartz
2007 ◽  
Vol 26 (9) ◽  
pp. 935-943 ◽  
Author(s):  
Akiko Makiuchi ◽  
Kazuhiro Yamaura ◽  
Shinya Mizuno ◽  
Kunio Matsumoto ◽  
Toshikazu Nakamura ◽  
...  

2010 ◽  
Vol 120 (11) ◽  
pp. 437-443
Author(s):  
Ewa Kwiatkowska ◽  
Karolina Kędzierska ◽  
Joanna Bober ◽  
Barbara Dołęgowska ◽  
Violetta Dziedziejko ◽  
...  

Shock ◽  
1996 ◽  
Vol 5 ◽  
pp. 70
Author(s):  
Aml M. Raafat ◽  
Timothy McGuire ◽  
Michael DeFrain ◽  
Alexander P. Franko ◽  
Scott A. Dulchavsky ◽  
...  

2019 ◽  
Vol 317 (2) ◽  
pp. F229-F239 ◽  
Author(s):  
Yoei Miyabe ◽  
Sachiko Sekiya ◽  
Naoko Sugiura ◽  
Masatoshi Oka ◽  
Kazunori Karasawa ◽  
...  

Ischemia-reperfusion injury (IRI) is a clinically important cause of acute kidney injury leading to chronic kidney disease. Furthermore, IRI in renal transplantation still remains a risk factor for delayed graft function. Previous studies on IRI have had some limitations, and few of the studied therapies have been clinically applicable. Therefore, a new method for treating renal IRI is needed. We examined the effects of human mesothelial cell (MC) sheets and hepatocyte growth factor (HGF)-transgenic MC (tg MC) sheets transplanted under the renal capsule in an IRI rat model and compared these two treatments with the intravenous administration of HGF protein and no treatment through serum, histological, and mRNA analyses over 28 days. MC sheets and HGF-tg MC sheets produced HGF protein and significantly improved acute renal dysfunction, acute tubular necrosis, and survival rate. The improvement in necrosis was likely due to the cell sheets promoting the migration and proliferation of renal tubular cells, as observed in vitro. Expression of α-smooth muscle actin at day 14 and renal fibrosis at day 28 after IRI were significantly suppressed in MC sheet and HGF-tg MC sheet treatment groups compared with the other groups, and these effects tended to be reinforced by the HGF-tg MC sheets. These results suggest that the cell sheets locally and continuously affect renal paracrine factors, such as HGF, and support recovery from acute tubular necrosis and improvement of renal fibrosis in chronic disease.


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