Fibroblast Growth Factor-8 Inhibits Oxidative Stress-Induced Apoptosis In H9C2 Cells

Keywords

AKT; Apoptosis; FGF-8; FoxO-1; H9c2 cardiomyoblasts

Abstract

Fibroblast growth factors (FGFs) comprise a large family of signaling molecules that involve cell patterning, mobilization, differentiation, and proliferation. Various FGFs, including FGF-1, FGF-2, and FGF-5, have been shown to play a role in cytoprotection during adverse cardiac events; however, whether FGF-8 is a cytoprotective remains unclear. The current study was designed to evaluate the effect of FGF-8 treatment on oxidative stress-induced apoptosis in H9c2 cells. Cells were divided into three groups: control, H2O2 (400 µm H2O2), and H2O2 + FGF-8 (4 ng/ml FGF-8). Our results suggest apoptosis was significantly (p < 0.05) enhanced in the H2O2 group relative to control. Moreover, a significant (p < 0.05) decline in apoptosis was observed in the H2O2 + FGF-8 group compared to H2O2-treated cells as evidenced by TUNEL staining, a cell death detection ELISA, and cell viability. Levels of downstream apoptotic mediators, caspase-3 and caspase-9, were significantly (p < 0.05) upregulated following H2O2 treatment but were abrogated following FGF-8 application. Expression levels of Forkhead box protein O1 (FoxO-1), MnSOD, catalase, pAKT, and p-mTOR were significantly (p < 0.05) reduced in the H2O2 group (p < 0.05). Notably, these levels were significantly (p < 0.05) reversed following FGF-8 treatment. Our data, for the first time, suggest FGF-8 is an anti-apoptotic mediator in oxidative-stressed H9c2 cells. Furthermore, our data demonstrate that apoptotic inhibition by FGF-8 is consequent to FoxO-1 oxidative detoxification as well as augmentation to the PI3K/AKT cell survival pathway.

Publication Date

1-1-2017

Publication Title

Molecular and Cellular Biochemistry

Volume

425

Issue

1-2

Number of Pages

77-84

Document Type

Article

Personal Identifier

scopus

DOI Link

https://doi.org/10.1007/s11010-016-2863-2

Socpus ID

84994168921 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/84994168921

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