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Autophagy attenuates diabetic glomerular damage through protection of hyperglycemia-induced podocyte injury

Fang, Li ; Zhou, Yang ; Cao, Hongdi ; Wen, Ping ; Jiang, Lei ; He, Weichun ; Dai, Chunsun ; Yang, Junwei Rastaldi, Maria Pia

PloS one, 2013-04, Vol.8 (4), p.e60546-e60546 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Autophagy attenuates diabetic glomerular damage through protection of hyperglycemia-induced podocyte injury
Autor: Fang, Li ; Zhou, Yang ; Cao, Hongdi ; Wen, Ping ; Jiang, Lei ; He, Weichun ; Dai, Chunsun ; Yang, Junwei
Rastaldi, Maria Pia
Assuntos: Adenine - analogs & derivatives ; Adenine - pharmacology ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins - genetics ; Autophagy ; Autophagy - drug effects ; Autophagy - physiology ; Beclin-1 ; Biology ; Cell division ; Defects ; Diabetes ; Diabetes mellitus ; Diabetic nephropathies ; Diabetic Nephropathies - physiopathology ; Endoplasmic reticulum ; Endoplasmic Reticulum - metabolism ; Glucose ; Homeostasis ; Hospitals ; Hyperglycemia ; Hyperglycemia - complications ; Inhibition ; Kidney diseases ; Level (quantity) ; Levels ; Medicine ; Mice ; Nephropathy ; Pathogenesis ; Permeability ; Phagocytosis ; Podocytes - pathology ; Podocytes - physiology ; Proteins ; Quality control ; RNA, Small Interfering - genetics ; RNA, Small Interfering - pharmacology ; Rodents ; siRNA ; Studies ; Taurochenodeoxycholic Acid - pharmacology ; Tauroursodeoxycholic acid
É parte de: PloS one, 2013-04, Vol.8 (4), p.e60546-e60546
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Conceived and designed the experiments: JY CD. Performed the experiments: LF YZ HC PW. Analyzed the data: LF WH. Contributed reagents/materials/analysis tools: LJ. Wrote the paper: LF JY.
Competing Interests: The authors have declared that no competing interests exist.
Descrição: Despite the recent attention focused on the important role of autophagy in maintaining podocyte homeostasis, little is known about the changes and mechanisms of autophagy in podocyte dysfunction under diabetic condition. In this study, we investigated the role of autophagy in podocyte biology and its involvement in the pathogenesis of diabetic nephropathy. Podocytes had a high basal level of autophagy. And basal autophagy inhibition either by 3-methyladenenine (3-MA) or by Beclin-1 siRNA was detrimental to its architectural structure. However, under diabetic condition in vivo and under high glucose conditions in vitro, high basal level of autophagy in podocytes became defective and defective autophagy facilitated the podocyte injury. Since the dynamics of endoplasmic reticulum(ER) seemed to play a vital role in regulating the autophagic flux, the results that Salubrinal/Tauroursodeoxycholic acid (TUDCA) could restore defective autophagy further indicated that the evolution of autophagy may be mediated by the changes of cytoprotective output in the ER stress. Finally, we demonstrated in vivo that the autophagy of podocyte was inhibited under diabetic status and TUDCA could improve defective autophagy. Taken together, these data suggested that autophagy might be interrupted due to the failure of ER cytoprotective capacity upon high glucose induced unmitigated stress, and the defective autophagy might accelerate the irreparable progression of diabetic nephropathy.
Editor: United States: Public Library of Science
Idioma: Inglês

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Autophagy attenuates diabetic glomerular damage through protection of hyperglycemia-induced podocyte injury

Fang, Li ; Zhou, Yang ; Cao, Hongdi ; Wen, Ping ; Jiang, Lei ; He, Weichun ; Dai, Chunsun ; Yang, Junwei Rastaldi, Maria Pia

United States: Public Library of Science

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