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- Copyright
- © 2011 American Heart Association, Inc.
- ISSN
- 1079-5642
- eISSN
- 1524-4636
- DOI
- 10.1161/ATVBAHA.111.228924
- pmid
- 21617141
- Publisher site
- See Article on Publisher Site
Abstract
Knockout of Toll-Like Receptor-2 Attenuates Both the Proinflammatory State of Diabetes and Incipient Diabetic Nephropathy Sridevi Devaraj, Peter Tobias, Balakuntalam S. Kasinath, Rajendra Ramsamooj, Alaa Afify, Ishwarlal Jialal Objective—Type 1 diabetes (T1DM) is a proinflammatory state and confers an increased risk for vascular complications. Toll-like receptors (TLR) could participate in diabetic vasculopathies. Whether TLR activation contributes to the proinflammatory state of T1DM and the pathogenesis of diabetic nephropathy remains unknown. Methods and Results—We induced T1DM in TLR2 knockout mice (TLR2/) and wild-type littermates (C57BL/6J- WT) using streptozotocin (STZ). Fasting blood, peritoneal macrophages, and kidneys were obtained for flow cytometry, Western blot, microscopy, and cytokine assays at 6 and 14 weeks after induction of diabetes. Macrophage TLR2 expression and MyD88-dependent signaling were increased in diabetic mice (WTSTZ) compared with nondiabetic WT mice. These biomarkers were attenuated in diabetic TLR2/ macrophages. WTSTZ mice showed increased kidney:body weight ratio due to cell hypertrophy, increased albuminuria, decreased kidney nephrin, podocin, and podocyte number and increased transforming growth factor- and laminin compared with WT mice. Nephrin, podocin, and podocyte number and effacement were restored, and transforming growth factor- and laminin levels were decreased in TLR2/ STZ mice kidneys versus WTSTZ. Peritoneal and kidney macrophages
Journal
Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health
Published: Aug 1, 2011