Abstract
To evaluate proteins associated with the development of diabetic nephropathy, a major cause of the end-stage renal disease, we analyzed protein expression in isolated glomeruli from spontaneous type 2 diabetic (OLETF) rats and their age-matched control littermates (LETO) in the early and proteinuric stages of diabetic nephropathy using QSTAR Elite LC-MS/MS. Among the 191 and 218 proteins that were altered significantly in the OLETF rats, twenty-four were actin cytoskeleton-associated proteins implicated in the formation of stress fibers, and the impairment of actin polymerization, intermediate filaments and microtubules. Importantly, sorbin and SH3 domain containing 2 (SORBS2), which is involved in the formation of stress fibers, was significantly upregulated in both stages of diabetic nephropathy (1.49- and 1.97-fold, resp.). Immunohistochemical and quantitative-PCR analyses revealed upregulation of SORBS2 in podocytes of glomeruli of OLETF rats. Our findings suggested that SORBS2 may be associated with the development of diabetic nephropathy possibility by reorganization of actin filaments.
Highlights
Diabetes mellitus accounts for more cases of end-stage renal disease than any other cause of chronic kidney disease [1]
Our findings suggested that sorbin and SH3 domain containing 2 (SORBS2) may be associated with the development of diabetic nephropathy possibility by reorganization of actin filaments
Mesangial matrix expansion, and glomerular basement membrane (GBM) thickening are the classical hallmarks of diabetic glomerular lesions, studies of diabetic patients and animal models have revealed that the onset of proteinuria is most closely associated with podocytopathies, such as podocyte apoptosis, hypertrophy, detachment from the GBM, and foot process effacement [2]
Summary
Diabetes mellitus accounts for more cases of end-stage renal disease than any other cause of chronic kidney disease [1]. Mesangial matrix expansion, and glomerular basement membrane (GBM) thickening are the classical hallmarks of diabetic glomerular lesions, studies of diabetic patients and animal models have revealed that the onset of proteinuria is most closely associated with podocytopathies, such as podocyte apoptosis, hypertrophy, detachment from the GBM, and foot process effacement [2]. Diabetic nephropathy is recognized as one of the major podocyte-associated diseases [3]. The podocyte is an excellent model system for studying actin cytoskeleton dynamics in a physiological context because changes in actin dynamics transfer directly into changes of kidney function [4]. Reorganization of the actin filaments is indispensable for foot process effacement
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