First Author | Qi H | Year | 2020 |
Journal | Biochem Biophys Res Commun | Volume | 521 |
Issue | 1 | Pages | 190-195 |
PubMed ID | 31630796 | Mgi Jnum | J:292054 |
Mgi Id | MGI:6445449 | Doi | 10.1016/j.bbrc.2019.10.102 |
Citation | Qi H, et al. (2020) NORAD affects the progression of diabetic nephropathy through targeting miR-520h to upregulate TLR4. Biochem Biophys Res Commun 521(1):190-195 |
abstractText | To uncover the role of NORAD in the progression of diabetic nephropathy (DN) and the underlying mechanism. Relative levels of NORAD and TLR4 in db/m mice and db/db mice were tested. Meanwhile, their levels in glomerular mesangial cells undergoing high-level (H-MC group) or low-level (L-MC) glucose treatment were determined. Regulatory effects of NORAD and TLR4 on proliferative ability and apoptosis in SV40-MES-13cells were assessed. The interaction in the regulatory loop NORAD/miR-520h/TLR4 was verified through dual-luciferase reporter gene assay, determination of subcellular distribution and RIP (RNA Immunoprecipitation) assay. At last, potential role of the regulatory loop NORAD/miR-520h/TLR4 in regulating DN was clarified. NORAD and TLR4 were upregulated in db/db mice and SV40-MES-13cells in H-MC group. Overexpression of them promoted proliferative ability and inhibited apoptosis in SV40-MES-13cells. MiR-520h was confirmed to bind NORAD and TLR4. NORAD, miR-520h and TLR4 were mainly distributed in cytoplasm, which were enriched in anti-Ago2. The regulatory loop NORAD/miR-520h/TLR4 has been demonstrated to promote the progression of DN. The regulatory loop NORAD/miR-520h/TLR4 promotes the proliferative ability and inhibits apoptosis in glomerular mesangial cells, thus aggravating the progression of DN. |