Fig. 1

Increased miR-92a expression in crescents and podocytes during nephrotoxic nephritis and human crescentic glomerulonephritis. a Representative microRNA profiling on dynabeads-isolated glomeruli from control or NTS-challenged mice (NTN). Values are means ± s.e.m., *p < 0.05 vs. control condition (n = 3 samples per condition). b Relative abundance of miR-92a assessed by RT-qPCR in sorted podocytes from normal healthy mice (control) and NTS-challenged mice (NTN). Values are means ± s.e.m., *p < 0.05 vs. control condition (n = 5 mice per condition). c Double miR-92a in situ hybridization (blue staining) and WT1 staining (brown staining) of kidney sections from normal mice (control) and NTS-challenged mice (NTN). Pictures in the bottom show a higher magnification of the top panel. Scale bars, 10 μm. d miR-92a in situ hybridization of kidney sections from random biopsies from individuals diagnosed with non-crescentic glomerulopathies, including minimal change disease (MCD) and membranous nephropathy (MN), and from patients with RPGN of various etiologies including stage III and IV lupus nephritis (LN), microscopic polyangiitis (MPA), and granulomatosis with polyangiitis (GPA). Scale bars, 50 μm. The lower panel shows higher magnification of middle panels (black box). Black stars (*) show miR-92a-positive cells. e RT-qPCR analysis of the relative abundance of miR-92a in microdissected glomeruli from four patients with non-crescentic glomerulopathies (black bars) and six patients with crescentic RPGN (white bars). Values are means ± s.e.m., *p < 0.05 vs. non-crescentic glomerular diseases. f Fluorescent in situ hybridization of miR-92a (red) and WT1 (green) on patients biopsies described in d. Bottom panel shows higher magnification of top panel (white box). White arrows show colocalization of WT1-positive cells and miR-92a expression. Scale bars, 50 μm. Statistical analysis: Mann–Whitney test to compare two groups