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Hepatic expression profiling shows involvement of PKC epsilon, DGK eta, Tnfaip, and Rho kinase in type 2 diabetic nephropathy rats
Author(s) -
Gupta Jeena,
Gaikwad Anil Bhanudas,
Tikoo Kulbhushan
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22783
Subject(s) - diabetic nephropathy , protein kinase c , medicine , endocrinology , diabetes mellitus , nephropathy , immunohistochemistry , type 2 diabetes , streptozotocin , gene expression , kinase , gene expression profiling , gene , biology , microbiology and biotechnology , biochemistry
Type 2 diabetes is associated with an increased risk for developing fatty liver disease, which results in an increased incidence of diabetic nephropathy. Hence, the present study was conceived to identify transcriptional changes in the liver that can provide molecular mediators for increased risk of developing nephropathy associated with type 2 diabetes. Type 2 diabetes was rendered in male SD rats using both high‐fat diet and low dose of streptozotocin (35 mg/kg, intraperitonially, i.p.). Hepatic gene expression profiling was performed in animals after development of diabetic nephropathy. The gene expression data were validated by RT‐PCR, protein expression, and immunohistochemistry. Gene expression profiling data revealed dramatic increase in expression of PKC epsilon, TNF‐alpha‐induced protein (four‐ to seven‐folds), and decrease in the expression of DGK eta in the liver of diabetic nephropathic rats. Furthermore, there was an increase in expression of genes regulating Rho signaling pathway, which was further confirmed by increase in Rho kinase activity. To the best of our knowledge, this is the first report which shows the involvement of PKC epsilon, DGK eta, Tnfaip, and Rho kinase in the liver of type 2 diabetic rats and its association with diabetic nephropathy. J. Cell. Biochem. 111: 944–954, 2010. © 2010 Wiley‐Liss, Inc.