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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Biomed+Res+Int 2020 ; 2020 (ä): 3152043 Nephropedia Template TP
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Negative Regulation of Tec Kinase Alleviates LPS-Induced Acute Kidney Injury in Mice via theTLR4/NF-kappaB Signaling Pathway #MMPMID32685466
Zhang W; Zhou P; Jiang X; Fan Z; Xu X; Wang F
Biomed Res Int 2020[]; 2020 (ä): 3152043 PMID32685466show ga
Tec kinase is an important mediator in inflammatory immune response that enhances the activity of neutrophils and macrophages. However, information on its function in lipopolysaccharide- (LPS-) induced acute kidney injury (AKI) is limited. This study is aimed at determining whether Tec kinase was a regulator in AKI. An AKI model in mice was successfully established using intraperitoneal LPS. Results showed that the serum levels of creatinine (Cr), blood urea nitrogen (BUN), and cystatin-C (Cys-C) increased after intraperitoneal LPS injection. Renal tissue sustained significantly severe injury as measured by pathological scores. Pretreatment with LFM-A13 improved the function of the kidney in mice and decreased the renal injury score. Enzyme-linked immunosorbent assay showed that LFM-A13 significantly reduced the release of IL-1beta and TNF-alpha in mice exposed to LPS. LFM-A13 can evidently abrogate the expression of Tec protein, MyD88, TLR4, NF-kappaB p65, and Tec's phosphorylated protein as determined by Western blot. Immunohistochemistry analysis revealed that LFM-A13 markedly downregulated the expression of Tec kinase in renal tubular epithelial cells. In vitro, Tec kinase protein was expressed highly in NRK-52E cells after LPS exposure. Tec-siRNA also decreased IL-1beta and TNF-alpha production and obviously abolished phospho-p65 and phospho-IkappaBalpha expression in NRK-52E cell stimulated by LPS; however, Tec-siRNA increased the IkappaBalpha level. Altogether, these data suggested that Tec kinase can be a modulating protein in AKI through TLR4/NF-kappaB activation.