scholarly journals Cobalt chloride decreases fibroblast growth factor-21 expression dependent on oxidative stress but not hypoxia-inducible factor in Caco-2 cells

2012 ◽  
Vol 264 (2) ◽  
pp. 212-221 ◽  
Author(s):  
Yanlong Liu ◽  
Chunhong Wang ◽  
Yuhua Wang ◽  
Zhenhua Ma ◽  
Jian Xiao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cobalt Chloride ◽  
Hypoxia Inducible Factor ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth

scholarly journals Fibroblast Growth Factor 21 Ameliorates Hyperuricemic Nephropathy by Improving Oxidative Stress through Activating Akt/Nrf2 Signaling Pathway

2021 ◽  
Author(s):  
Xinghao Jiang ◽  
Yimeng Zou ◽  
Yeboah Kwaku Opoku ◽  
Shijie Liu ◽  
Dan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Therapeutic Effect ◽  
Knockout Mice ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Glomerular Mesangial Cells ◽  
Nrf2 Signaling Pathway

Abstract Epidemiological investigations have shown an elevated expression of fibroblast growth factor 21 (FGF21) in the serum of patients with hyperuricemia. However, the effect of FGF21 on hyperuricemic nephropathy is still unknown. The purpose of this study, therefore, was to explore the effect and mechanism of action of FGF21 on hyperuricemic nephropathy. The level of FGF21 in PBMCs was determined in 10 patients with hyperuricemic nephropathy. Hyperuricemic mice models were induced in wild-type C57BL/6 and FGF21 knockout mice. Six mice in each group were treated with FGF21 at a dose of 1mg/kg and 5mg/kg for 30 days. For the in vitro studies, glomerular mesangial cells were exposed to lipopolysaccharide and monosodium uric acid to induce inflammation. This was followed by treatment with 100nM, 1000nM of FGF21 for 72 h to observe the therapeutic effect. The levels of FGF21 in patients with hyperuricemic nephropathy were elevated. Also, FGF21 knockout mice experienced more severe nephropathy compared to the WT mice. This was characterized by an increase in inflammatory factors and fibrosis in the kidney, which was reversed by exogenous FGF21 treatment. FGF21 recorded a significant therapeutic effect through the activation of Akt/Nrf2 signal pathway in both in vivo and in vitro studies. However, the effect increasing effect of FGF21 on Nrf2 was reduced by the addition of Akt inhibitor GSK690693. In conclusion, our study found for the first time that FGF21 can significantly improve hyperuricemic nephropathy through the promotion of the Akt/Nrf2 signalling pathway leading to improvement in oxidative stress.

scholarly journals Fibroblast Growth Factor 21 Protects Against Atrial Remodeling via Reducing Oxidative Stress

2021 ◽  
Vol 8 ◽  
Author(s):  
Miao Chen ◽  
Jiawei Zhong ◽  
Zhen Wang ◽  
Hongfei Xu ◽  
Heng Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 21 ◽  
Atrial Remodeling ◽  
Protective Effects ◽  
Fibroblast Growth ◽  
Atrial Myocytes ◽  
Antioxidant Genes

Aim: The structural and electrical changes in the atrium, also known as atrial remodeling, are the main characteristics of atrial fibrillation (AF). Fibroblast growth factor 21 (Fgf21) is an important endocrine factor, which has been shown to play an important role in cardiovascular diseases. However, the effects of Fgf21 on atrial remodeling have not been addressed yet. The purpose of the present study is to evaluate the effects of Fgf21 on atrial remodeling.Methods and Results: Adult mice were treated with Ang II, and randomly administrated with or without Fgf21 for 2 weeks. The susceptibility to AF was assessed by electrical stimulation and optical mapping techniques. Here, we found that Fgf21 administration attenuated the inducibility of atrial fibrillation/atrial tachycardia (AF/AT), improved epicardial conduction velocity in the mice atria. Mechanistically, Fgf21 protected against atrial fibrosis and reduced oxidative stress of the atria. Consistently, in vitro study also demonstrated that Fgf21 blocked the upregulation of collagen by Tgf-β in fibroblasts and attenuated tachypacing-induced oxidative stress including reactive oxygen species (ROS), Tgf-β, and ox-CaMKII in atrial myocytes. We further found that Fgf21 attenuated oxidative stress by inducing antioxidant genes, such as SOD2 and UCP3. Fgf21 also improved tachypacing-induced myofibril degradation, downregulation of L-type calcium channel, and upregulation of p-RyR2, which implicated protective effects of Fgf21 on structural and electrical remodeling in the atria. Moreover, Nrf2 was identified as a downstream of Fgf21 and partly mediated Fgf21-induced antioxidant gene expression in atrial myocytes.Conclusion: Fgf21 administration effectively suppressed atrial remodeling by reducing oxidative stress, which provides a novel therapeutic insight for AF.

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.

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