PloS one, 2017-03, Vol.12 (3), p.e0174471-e0174471
2017
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- Autor(en) / Beteiligte
- Titel
- SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy
- Ist Teil von
- PloS one, 2017-03, Vol.12 (3), p.e0174471-e0174471
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2017
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Progressive reduction of SnoN is associated with gradual elevation of TGF-β1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-β1 signaling, with potential therapeutic benefits against TGF- β1 -induced renal fibrosis. To characterize SnoN for its role in renal fibrosis, we assessed SnoN expression patterns in response to high glucose stress, and evaluated the effects of upregulating SnoN on renal fibrosis. High glucose stress induced significantly elevated SnoN, TGF-β1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions. Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis. Alternatively, EMT was suppressed by dominantly expressed exogenous SnoN without interfering with TGF-β1. Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0174471Titel-ID: cdi_plos_journals_1882247895
- Format
- –
- Schlagworte
- Actin, Analysis, Animals, Antibodies, Biochemistry, Biology and life sciences, Blocking, Blood, Blotting, Western, Cadherins - genetics, Cadherins - metabolism, Cadmium, Cancer, Carbon dioxide, Care and treatment, Cell culture, Cell Line, Chemokines, Citric acid, Computer programs, Cybernetics, Cytokines, Degradation, Diabetes, Diabetes mellitus, Diabetes Mellitus, Experimental - genetics, Diabetes Mellitus, Experimental - metabolism, Diabetic nephropathies, Diabetic Nephropathies - genetics, Diabetic Nephropathies - metabolism, Diabetic nephropathy, Diagnosis, Effectors, Epithelial Cells - drug effects, Epithelial Cells - metabolism, Epithelial-Mesenchymal Transition - drug effects, Epithelial-Mesenchymal Transition - genetics, Fasting, Fibrosis, Fibrosis - genetics, Fibrosis - metabolism, Fluorescent antibody technique, Glucose, Glucose - metabolism, Glucose - pharmacology, Growth factors, Health aspects, Hematology, Hills, Hospitals, Humans, Immune system, Immunoglobulins, Incidence, Inhibition, Injection, Intervention, Ischemia, Kidney - drug effects, Kidney - metabolism, Kidney - pathology, Kidney diseases, Kidney Tubules, Proximal - drug effects, Kidney Tubules, Proximal - metabolism, Kinases, Male, Medical research, Medicine and Health Sciences, Metabolism, Metastases, Metastasis, Mice, Milk, Modulation, Nephrology, Nephropathy, Nerve Tissue Proteins - genetics, Nerve Tissue Proteins - metabolism, Physical Sciences, Physiological effects, Proteins, Quality, Rats, Rats, Sprague-Dawley, Regulators, Renal failure, Renal function, Research and Analysis Methods, Reverse Transcriptase Polymerase Chain Reaction, Ribonucleic acid, Risk factors, RNA, RNA Interference, Rodents, Signal transduction, Smooth muscle, Sodium, Spring (season), Temperature effects, Transcription Factors - genetics, Transcription Factors - metabolism, Transcriptional Activation - drug effects, Transforming Growth Factor beta1 - genetics, Transforming Growth Factor beta1 - metabolism, Transforming growth factor-b1, Transforming growth factors, Ubiquitin-Protein Ligases - genetics, Ubiquitin-Protein Ligases - metabolism, Up-Regulation, Vasoactive agents