title: Overexpression of toll-like receptor 2 in glomerular endothelial cells and podocytes in septic acute kidney injury mouse model.
abstract: Acute kidney injury (AKI) is one of the most common complications in patients with severe sepsis. The development of septic AKI increases patients' mobility and even mortality. Toll-like receptor 2 (TLR2), as a membrane surface receptor for bacterial, fungal, viral and certain endogenous substances, has been described to contribute to the development of septic AKI; however, the renal cell types associating TLR2 overactivation in septic AKI has not been described. In the current study, we investigated the TLR2 activation patterns in the kidney of lipopolysaccharide-induced septic AKI mice. Our results demonstrated that mRNA level of TLR2 significantly increased in the kidney of lipopolysaccharide-treated mice. Immunohistochemistry revealed the overactivation of TLR2 in the glomeruli. Double immunofluorescence analysis shows the precise distribution of TLR2 by showing the colocalization of TLR2 in glomeruli with synaptopodin, a podocyte marker, and Tie2, an endothelial marker. In addition, proapoptotic molecules Bax and Caspase-3 were increased in the glomeruli of lipopolysaccharide-treated mice. Together, the current study indicates that TLR2 is overactivated in the glomerular endothelial cells and podocytes in septic AKI mice, while the abundance of Bax and Caspase-3 were increased in the glomeruli of these mice, it may supply a clue that TLR2 induced these cell apoptosis in AKI. This finding provides an alternative mechanism to understand AKI development and potential targets for treatment.
authors.affiliation: Intensive Care Unit, The First people's Hospital of Kunshan , Jiangsu Province , China .
authors.forename: Yuan
authors.initials: Y
authors.lastname: Peng
authors.forename: Xi
authors.initials: X
authors.lastname: Zhang
authors.forename: Yongfang
authors.initials: Y
authors.lastname: Wang
authors.forename: Shasha
authors.initials: S
authors.lastname: Li
authors.forename: Junlei
authors.initials: J
authors.lastname: Wang
authors.forename: Long
authors.initials: L
authors.lastname: Liu
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000166:cytology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D050199:Podocytes / Q000378:metabolism*; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis*
chemical_list: D051195:Toll-Like Receptor 2
keywords: Acute kidney injury; Toll-like receptor 2; glomerular endothelial cell; podocyte; sepsis