miR-200bc/429 cluster alleviates inflammation in IgA nephropathy by targeting TWEAK/Fn14 |
| |
| Institution: | 1. State Key Laboratory of Kidney Diseases, Department of Urology, Chinese People’s Liberation Army Medical School, Chinese People’s Liberation Army General Hospital, Beijing, P.R. China;2. Medical School, Nankai University, Tianjin, P.R. China;1. Cardiology Service, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain;2. Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain;3. Christchurch Heart Institute, University of Otago, Christchurch, New Zealand;4. Cardiovascular Research Institute, National University of Singapore, Singapore, Singapore;5. Coronary Care Unit and Heart Failure Program, VA San Diego, San Diego, California;6. University of California San Diego, San Diego, California;7. Department of Cardiology, University Hospital Basel, Basel, Switzerland;8. Cardiovascular Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania;9. Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania;1. Department of Dermatology, Hôpital Cochin, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France;2. Université de Paris, Faculté de médecine, 15, rue de L’École-de-Médecine, 75006 Paris, France;3. Biologie Cutanée, Institut Cochin, Inserm UMRS 1016, 22, rue Mechain, 75014 Paris, France |
| |
| Abstract: | Immunoglobulin A nephropathy (IgAN) is one of the most common glomerular diseases worldwide. Various studies have identified a host of microRNAs (miRNAs) abnormally expressed in IgAN and might affect the pathogenesis and progression of IgAN. However, miR-200bc/429 cluster in the pathopoiesis of IgAN remains poorly understood. For this study, we found that miR-200bc/429 cluster is downregulated in IgAN tissues and IgAN podocytes and HK2 cells compared with their matched controls respectively. In addition, overexpression of miR-200bc/429 cluster in IgAN podocytes and HK2 cells could attenuate the release of inflammatory cytokines MCP-1, IL-6 and RANTES. Moreover, the 3′ untranslated region (UTR) of TNF-like weak inducer of apoptosis (TWEAK) was identified to be a direct target of miR-200bc/429 cluster. Furthermore, our results showed that miR-200bc/429 cluster can inhibit TWEAK mediated NF-κB pathway activation in IgAN. Overall, our findings revealed that miR-200bc/429 cluster alleviates inflammation in IgAN through TWEAK/Fn14 system and might serve as a biomarker as well as a promising therapeutic target for IgAN. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
