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  • Title: miR-129-5p alleviates LPS-induced acute kidney injury via targeting HMGB1/TLRs/NF-kappaB pathway.
    Author: Huang X, Hou X, Chuan L, Wei S, Wang J, Yang X, Ru J.
    Journal: Int Immunopharmacol; 2020 Dec; 89(Pt A):107016. PubMed ID: 33039954.
    Abstract:
    INTRODUCTION: The present study aimed to investigate whether miR-129-5p can regulate high-mobility group box protein 1 (HMGB1)-modulated TLRs/NF-kappaB inflammatory pathway that contributed to lipopolysaccharide (LPS)-induced podocyte apoptosis and acutekidneyinjury (AKI). MATERIAL AND METHODS: In vitro and in vivo models of sepsis were simulated using LPS-administrated podocytes and mice, respectively. The effects of LPS, mR-129-5p mimics and short hairpin RNA of HMGB1 (sh-HMGB1) on podocyte apoptosis were monitored using TUNEL staining. Protein expression was measured using western blotting. Survival outcomes were analyzed in septic mice with agomir-mR-129-5p administration. RESULTS: We observed that stimulation of podocytes with LPS significantly inhibits the expression of miR-129-5p, and overexpression of miR-129-5p protects against LPS-induced podocyte damage, over-activation of inflammatory response and apoptosis. In a mouse model, agomir-miR-129-5p administration significantly improves the survival outcomes in septic mice and LPS-induced AKI. Mechanically, LPS-induced the elevation of HMGB1, TLR2, TLR4 and nuclear NF-κB protein expression in vitro and in vivo are restrained by the overexpression of miR-129-5p. CONCLUSIONS: Overexpression of miR-129-5p protects against LPS-induced podocyte apoptosis, inflammation and AKI in vivo and in vitro models of sepsis. The underlying molecular mechanism is mediated via attenuating HMGB1/TLRs/NF-κB signaling axis modulated inflammatory response.
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