Fibroblast growth factor-8 inhibits oxidative stress-induced apoptosis in H9c2 cells

2016 ◽  
Vol 425 (1-2) ◽  
pp. 77-84 ◽  
Author(s):  
Reetu D. Singla ◽  
Jing Wang ◽  
Dinender K. Singla
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
H9c2 Cells ◽  
Fibroblast Growth Factor 8 ◽  
Induced Apoptosis

Proteomic study on the protective mechanism of fibroblast growth factor 21 to ischemia–reperfusion injury

2013 ◽  
Vol 91 (11) ◽  
pp. 973-984 ◽  
Author(s):  
Wei-Tao Cong ◽  
Jin Ling ◽  
Hai-Shan Tian ◽  
Ren Ling ◽  
Yang Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Energy Supply ◽  
Ischemia Reperfusion ◽  
Fibroblast Growth Factor 21 ◽  
Protective Mechanism ◽  
Fibroblast Growth ◽  
H9c2 Cells ◽  
Gsk 3Β

Fibroblast growth factor (FGF)-21 is a novel regulator of insulin-independent glucose transport in 3T3-L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. In this study, we found that FGF-21 can significantly attenuate ischemia–reperfusion (I/R) induced damage in H9c2 cells (rat heart). However, it is unclear which signal transduction pathway is involved in the cardioprotective effect of FGF-21. Thus, this study was designed to investigate the potential mechanism induced by FGF-21. The results showed that FGF-21 treatment prevented the oxidative stress and apoptosis associated with I/R damage by reducing the levels of superoxide anions, inhibiting glycogen synthase kinase (GSK) 3β by activating Akt phosphorylation, and recovering the levels of ATP synthase pyruvate kinase isozymes M1 and protein kinase C, thereby improving energy supply. In summary, we conclude that FGF-21 protects H9c2 cells against I/R injury mainly through the Akt–GSK-3β–caspase-3 dependent pathway, preventing oxidative stress, and recovery of the energy supply.

Methylcobalamin Inhibits Fibroblast Growth Factor-8 Stimulated Proliferation and Induces Apoptosis in Shionogi Carcinoma Cells

2008 ◽  
Vol 78 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Goto ◽  
Katayama ◽  
Tanigaki ◽  
Fushiki ◽  
Nishizawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Thymidine Incorporation ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Fibroblast Growth ◽  
Mammary Carcinoma Cell ◽  
Fibroblast Growth Factor 8 ◽  
Exogenous Addition ◽  
Induced Apoptosis

SC-3 cells, an androgen-dependent mouse mammary carcinoma cell line, in response to androgen stimuli, induces the secretion of fibroblast growth factor (FGF-8), which in turn increases the proliferation of these cells. We have shown previously that methylcobalamin (MeCbl) decreases the levels of FGF-8 mRNA in SC-3 cells stimulated by testosterone, inhibiting the proliferation of SC-3 cells and inducing apoptosis. In the present study, we analyzed the effects of MeCbl on SC-3 cell proliferation in response to exogenous addition of FGF-8. Thymidine incorporation showed a significant decrease in SC-3 cells cultured with MeCbl. Immunocytochemistry for single-stranded DNA (ssDNA) and DNA fragmentation analysis demonstrated that MeCbl induced apoptosis in SC-3 cells, even in the presence of FGF-8. These results show that the addition of FGF-8 stimulates the proliferation of SC-3 cells under the androgen-depleted condition and that MeCbl might be able to interfere with FGF-8 action.

Up-regulation of the fibroblast growth factor 8 subfamily in human hepatocellular carcinoma for cell survival and neoangiogenesis

Hepatology ◽  
2011 ◽  
Vol 53 (3) ◽  
pp. 854-864 ◽  
Author(s):  
Christine Gauglhofer ◽  
Sandra Sagmeister ◽  
Waltraud Schrottmaier ◽  
Carina Fischer ◽  
Chantal Rodgarkia-Dara ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Cell Survival ◽  
Fibroblast Growth Factor ◽  
Human Hepatocellular Carcinoma ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 8
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