Levels of Snhg1 were Increased in DN renal tissues and HG-treated MCs.

Snhg1 enhances inflammatory cytokine expression and promotes MC proliferation.

Snhg1 functions as a miR-27b sponge, consequently regulating KDM6B expression.

Snhg1 regulates the inflammatory-cytokine expression and MC proliferation via the miR-27b–KDM6B axis.

Diabetic nephropathy (DN) is the direct cause of end-stage renal disease, and nephritic inflammation plays a role in its growth and advancement. Aberrant expression of long non-coding RNAs (lncRNAs) correlates with many diseases, including DN. In this study, we investigated whether lncRNA small nucleolar RNA host gene 1 (Snhg1) was mechanistically involved in inflammation and mesangial cell (MC) proliferation in DN. We found that Snhg1 was significantly upregulated in DN renal tissues and high glucose (HG)-treated MCs. Overexpression of Snhg1 promoted inflammatory cytokine expression in MCs and MC proliferation under low-glucose conditions; meanwhile, Snhg1 knockdown suppressed inflammatory cytokine production and MC proliferation under HG conditions. Mechanistically, Snhg1 was found to directly bind miR-27b, thereby preventing the miRNA from binding its target KDM6B mRNA. Furthermore, miR-27b overexpression recapitulated the inhibitory effects of Snhg1 knockdown, whereas restoration of Snhg1 expression attenuated the function of miR-27b in MCs under HG conditions. Taken together, these results indicate that suppression of Snhg1 inhibited HG-induced inflammation and proliferation of MCs by regulating the miR-27b/KDM6B axis.

Diabetic nephropathy

LncRNA Snhg1

Inflammation

Proliferation

Mesangial cells

long non-coding RNA

small nucleolar RNA host gene 1

small interfering RNA

fluorescence in situ hybridization

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