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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ding, Yan Kim, Sung ll Lee, So-Young Koo, Ja Kun Wang, Zhibo Choi, Mary E. |
| Description | Author Affiliation: Ding Y ( Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts); Kim Sl ( Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts); Lee SY ( Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts); Koo JK ( Division of Nephrology and Hypertension, Weill Cornell Medical College, New York, New York); Wang Z ( Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts); Choi ME ( Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts) |
| Abstract | Autophagy is an evolutionarily conserved process that cells use to degrade and recycle cellular proteins and remove damaged organelles. During the past decade, there has been a growing interest in defining the basic cellular mechanism of autophagy and its roles in health and disease. However, the functional role of autophagy in kidney fibrosis remains poorly understood. Here, using GFP-LC3 transgenic mice, we show that autophagy is induced in renal tubular epithelial cells (RTECs) of obstructed kidneys after unilateral ureteral obstruction (UUO). Deletion of LC3B (LC3(-/-) mice) resulted in increased collagen deposition and increased mature profibrotic factor TGF-ß levels in obstructed kidneys. Beclin 1 heterozygous (beclin 1(+/-)) mice also displayed increased collagen deposition in the obstructed kidneys after UUO. We also show that TGF-ß1 induces autophagy in primary mouse RTECs and human renal proximal tubular epithelial (HK-2) cells. LC3 deficiency resulted in increased levels of mature TGF-ß in primary RTECs. Under conditions of TGF-ß1 stimulation and autoinduction, inhibition of autolysosomal protein degradation by bafilomycin A1 increased mature TGF-ß protein levels without alterations in TGF-ß1 mRNA. These data suggest a novel intracellular mechanism by which mature TGF-ß1 protein levels may be regulated in RTECs through autophagic degradation, which suppresses kidney fibrosis induced by UUO. The dual functions of TGF-ß1, as an inducer of TGF-ß1 autoinduction and an inducer of autophagy and TGF-ß degradation, underscore the multifunctionality of TGF-ß1. |
| File Format | HTM / HTML |
| ISSN | 10466673 |
| e-ISSN | 15333450 |
| DOI | 10.1681/ASN.2013101068 |
| Journal | Journal of the American Society of Nephrology |
| Issue Number | 12 |
| Volume Number | 25 |
| Language | English |
| Publisher | American Society of Nephrology |
| Publisher Date | 2014-12-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Nephrology Autophagy Fibrosis Pathology Kidney Diseases Metabolism Kidney Transforming Growth Factor Beta1 Ureteral Obstruction Animals Apoptosis Apoptosis Regulatory Proteins Genetics Collagen Heterozygote Kidney Tubules, Proximal Mice Mice, Inbred C57bl Mice, Transgenic Microtubule-associated Proteins Research Support, N.i.h., Extramural |
| Content Type | Text |
| Resource Type | Article |
| Subject | Nephrology |
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