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FGF20 relieves high glucose-induced Schwann cell mitochondrial damage through the activation of SIRT1
Ya Ning1, Yuewei Liang1, Youqing Huang2
1Pain Management Department, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Background:
Schwann cell mitochondrial damage plays an important role in diabetic neuropathic pain (DNP). Fibroblast growth factor 20 (FGF20) has been shown to protect nerve cells and regulate neural function, but its function and mechanism in DNP remain unclear.
Methods:
A DNP mouse model induced by streptozotocin (STZ) and an RSC96 cell model induced by high glucose (HG) were used for experimental studies. The metabolism of the mice was evaluated by measuring body weight and blood glucose levels. Pathological changes in the sciatic nerve were observed by hematoxylin and eosin (HE) staining. The pain sensitivity of the mice was evaluated by the von Frey test and thermal sensitivity test. Cell viability was determined by a cell counting kit-8 (CCK-8) assay. MitoSOX Red staining was performed to detect mitochondrial reactive oxygen species (ROS) levels. 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-benzimidazolyl carbocyanine iodide (JC-1) staining was used to measure the mitochondrial membrane potential, and the expression of proteins was detected by western blotting and immunohistochemistry.
Results:
FGF20 expression was low in DNP mice and HG-induced Schwann cells. Overexpression of FGF20 relieved symptoms in DNP mice, including partial recovery of body weight, a reduction in blood glucose levels, an increase in the tactile response threshold, and a reduction in thermal response delay. In addition, FGF20 overexpression increased the expression of the mitochondrial autophagy proteins PINK1 and Parkin, adenosine triphosphate (ATP) content, and mitochondrial membrane potential levels, and reduced ROS accumulation in RSC96 cells. Molecular mechanisms reveal that sirtuin 1 (SIRT1) expression is downregulated in DNP, and FGF20 upregulates SIRT1 expression, and that SIRT1 knockdown weakened the improvement effect of FGF20 on mitochondrial autophagy and damage.
Conclusion:
FGF20 may promote mitochondrial autophagy in Schwann cells by upregulating SIRT1 expression, thereby inhibiting mitochondrial damage and thus alleviating DNP.
