The Regulation of mRNA Demethylase Fat Mass and Obesity-associated Protein on Inflammatory Factors and Neutrophil Cytosolic Factor 2 Expression

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Abstract Title *

The Regulation of mRNA Demethylase Fat Mass and Obesity-associated Protein on Inflammatory Factors and Neutrophil Cytosolic Factor 2 Expression

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Co-author 1

Weihua Liu lwh10280465@163.com Fuzhou University Affiliated Provincial Hospital Department of Nephrology Fuzhou China *

Co-author 2

Tong Chen 498865059@qq.com Xinqiao Hospital Department of Nephrology Chongqing China -

Co-author 3

Miao Lin 10151246@qq.com Fuzhou University Affiliated Provincial Hospital Department of Nephrology Fuzhou China -

Co-author 4

Miao Zheng 804814250@qq.com Fujian University of Traditional Chinese Medicine Department of Nephrology Fuzhou China -

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Introduction

Acute kidney injury (AKI) is a serious clinical disorder with high mortality. Parenchymal cell injury, inflammatory cell infiltration, and fibrosis in renal tissues are the main pathological consequences. However, the involved molecular mechanisms remain to be fully elucidated. This study aims to explore the roles of mRNA demethylase in the oxidative stress and inflammation of renal cells

Methods

An oxygen-glucose deprivation and reoxygenation (OGD/R) treatment in HK-2 tubular epithelial cells was performed to mimic the ischemia-reperfusion injury in vivo. The effects of silencing fat mass and obesity-associated protein (FTO) expression and overexpressing neutrophil cytosolic factor 2 (NCF2) gene on oxidative stress, inflammatory factors, cell viability, and proliferation were investigated in HK-2 cells

Results

OGD/R increased the expression of IL-17A, CX3CL1, KLK10, KRT17, MMP1 and NCF2, but decreased CCL5, IGFBP6, and ISG15 mRNA expression with no effect on IL-17RA mRNA expression. The expression of IL-17-regulated gene CX3CL1 and ISG15 was increased, but KRT17 expression was decreased in HK-2 cells after silencing FTO gene. The level of TNF-α, LDH, and IL-18 was significantly downregulated after the knockdown of FTO gene. FTO knockdown also obviously decreased NLRP3, caspase-1, and ASC protein expression, whereas OGD/R significantly increased NLRP3, caspase-1, and ASC protein expression. Meclofenamic acid significantly inhibited the expression of FTO, NCF2, ASC, NLRP3 and caspase-1 protein. NCF2 overexpression significantly decreased TNF-α level, and increased LDH level without effect on IL-18 level in HK-2 culture supernatant. Overexpression of NCF2 decreased ASC, NLRP3, and IL-18 protein expression in HK-2 cells.

Conclusion

FTO gene is widely involved in the pathology of AKI through regulating IL-17 associated inflammatory signaling pathway and other inflammatory factors as well as oxidative stress.

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