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Aim @@@ The aim of the present study was to identify the regulatory relationship between miR-326-3p and FcRIII, and to explore the involvement of miR-326-3p/FcRIII/TGF-/Smad signalling pathway in fibrotic injury, which was induced by the high glucose (HG) and oxidized low density lipoprotein immune complex (ox-LDL-IC) in mouse glomerular mesangial cells (GMCs). @@@ MethodsResultsDual-luciferase reporter system and real time PCR (RT-PCR) were used to identify FcRIII as a target gene of miR-326-3p. Lentiviral transduction was used to construct different expression of miR-326-3p in GMCs, which were divided into three groups: miR-326-3p mimics group (miR-326-3p group), miR-326-3p inhibitor group (miR-326-3p-inhibit group) and scramble control group (control group). Then, each group was stimulated by normal glucose (NG), HG, ox-LDL-IC and HG+ox-LDL-IC, respectively. RT-PCR and western blot were used to measure the expressions of Col-I, CTGF, -SMA, TGF-, Smad2/3 and pSmad2/3. @@@ FcRIII was regulated negatively by miR-326-3p in GMCs under the condition of HG and ox-LDL-IC, which implied FcRIII as a target gene of miR-326-3p. Furthermore, compared with normal glucose group, the expressions of Col-I, CTGF, -SMA, TGF- and pSmad2/3 were higher under the condition of HG, ox-LDL-IC and HG+ox-LDL-IC (P<0.05). In particular, miR-326-3p-inhibit groups exhibited the most significant increase (P<0.05), while miR-326-3p could attenuate the increase (P<0.05). @@@ ConclusionSummary at a GlanceFcRIII was identified as a target gene of miR-326-3p. MiR-326-3p/FcRIII/TGF-/Smad signaling pathway was investigated to be involved in the pathophysiology of renal fibrosis of DKD. @@@ The study by Wang et al., investigated the interaction of microRNA-326-3p with IgG FcyRIII and implicates this interaction in fibrosis in glomerular mesangial cells in the context of diabetes.
- 出版日期2018-11
- 单位四川大学
