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Abstract: PO0936

IL-17A Deficiency Attenuates Autophagosome Formation in Streptozotocin-Induced Rat Diabetic Nephropathy

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic

Authors

  • Hong, Geum-Lan, Department of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Daejeon, Korea (the Republic of)
  • Kim, Kyung-hyun, Department of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Daejeon, Korea (the Republic of)
  • Jung, Ju young, Department of Veterinary Medicine & Institute of Veterinary Science, Chungnam National University, Daejeon, Korea (the Republic of)
Background

Diabetic nephropathy (DN) is one of the most important medical complications in diabetes mellitus. Autophagy is an important mediator of pathological responses and plays critical roles in inflammation during the progression of diabetic nephropathy. The Th-17 effector cytokine interleukin (IL)-17A can favorably modulate inflammatory disorders including DN. In this study, we examined whether IL-17A deficiency affects the autophagy process in streptozotocin (STZ)-induced DN in kidney.

Methods

The autophagic response for IL-17A in the nephrotoxicity of STZ was evaluated by observing STZ-induced functional and histological renal injury in IL-17a-/-mice.

Results

IL-17A KO STZ-treated mice were developed more severe nephropathy, exhibiting increased albuminuria, glomerular damage and renal interstitial fibrosis at 12 weeks. IL-17A deficiency also increase the up-regulation of proinflammatory cytokine and fibrotic genes expression after STZ treatment. Meanwhile, autophagy-associated proteins were induced in STZ wild type mice however, IL-17A KO STZ-treated mice displayed a significant decrease in these protein expression. Especially, LC3 and ATG7, which play crucial role for autophagosome formation, is notably decreased in IL-17A KO STZ-treated mice compared with their wild type counterparts.

Conclusion

These results suggested that autophagy is closely related to the increased cellular stress due to IL-17A deficiency. Our study demonstrate an important role of IL17A for autophagosome formation during the progression of DN and provide a potential therapeutic target for DN

Funding

  • Clinical Revenue Support