Downregulation of miR‐1224 protects against oxidative stress‐induced acute liver injury by regulating hepatocyte growth factor

2019 ◽  
Vol 120 (8) ◽  
pp. 12369-12375 ◽  
Author(s):  
Wenting Cheng ◽  
Guo‐pan Liu ◽  
Dehua Kong ◽  
Wei Huang ◽  
Ying Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Liver Injury ◽  
Hepatocyte Growth Factor ◽  
Acute Liver Injury ◽  
Hepatocyte Growth

Suppression of acute hepatic injury by a synthetic prostacyclin agonist through hepatocyte growth factor expression

2012 ◽  
Vol 302 (4) ◽  
pp. G420-G429 ◽  
Author(s):  
Qing Xu ◽  
Mizuho Nakayama ◽  
Yoshinori Suzuki ◽  
Katsuya Sakai ◽  
Takahiro Nakamura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Injury ◽  
Hepatocyte Growth Factor ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Protective Action ◽  
Liver Cells ◽  
Cyclooxygenase 2 ◽  
Peroral Administration ◽  
Hepatocyte Growth

Previous studies have demonstrated that mice disrupted with the cyclooxygenase-2 gene showed much more severe liver damage compared with wild-type mice after liver injury, and prostaglandins (PGs) such as PGE1/2 and PGI2 have decreased hepatic injury, but the mechanisms by which prostaglandins exhibit protective action on the liver have yet to be addressed. In the present study, we investigated the mechanism of the protective action of PGI2 using the synthetic IP receptor agonist ONO-1301. In primary cultures of hepatocytes and nonparenchymal liver cells, ONO-1301 did not show protective action directly on hepatocytes, whereas it stimulated expression of hepatocyte growth factor (HGF) in nonparenchymal liver cells. In mice, peroral administration of ONO-1301 increased hepatic gene expression and protein levels of HGF. Injections of CCl4 induced acute liver injury in mice, but the onset of acute liver injury was strongly suppressed by administration of ONO-1301. The increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) by CCl4 were suppressed by 10 mg/kg ONO-1301 to 39.4 and 33.6%, respectively. When neutralizing antibody against HGF was administered with ONO-1301 and CCl4, the decreases by ONO-1301 in serum ALT and AST, apoptotic liver cells, and expansion of necrotic areas in liver tissue were strongly reversed by neutralization of endogenous HGF. These results indicate that ONO-1301 increases expression of HGF and that hepatoprotective action of ONO-1301 in CCl4-induced liver injury may be attributable to its activity to induce expression of HGF, at least in part. The potential for involvement of HGF-Met-mediated signaling in the hepatotrophic action of endogenous prostaglandins generated by injury-dependent cyclooxygenase-2 induction is considerable.

CCl4 -induced acute liver injury in mice is inhibited by hepatocyte growth factor overexpression but stimulated by NK2 overexpression

FEBS Letters ◽  
2002 ◽  
Vol 532 (3) ◽  
pp. 391-395 ◽  
Author(s):  
Toshiyuki Otsuka ◽  
Hitoshi Takagi ◽  
Norio Horiguchi ◽  
Mitsuo Toyoda ◽  
Ken Sato ◽  
...  
Keyword(s):  
Growth Factor ◽  
Liver Injury ◽  
Hepatocyte Growth Factor ◽  
Acute Liver Injury ◽  
Hepatocyte Growth

Oxidative stress contributes to hepatocyte growth factor-dependent pro-senescence activity of ovarian cancer cells

2017 ◽  
Vol 110 ◽  
pp. 270-279 ◽  
Author(s):  
Justyna Mikuła-Pietrasik ◽  
Paweł Uruski ◽  
Martyna Pakuła ◽  
Konstantin Maksin ◽  
Sebastian Szubert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ovarian Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Hepatocyte Growth
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