Fig. 1

Renal ECM expression and MDSC distribution in STZ-treated diabetic mice. a Diabetes induced in mice using one dose of streptozotocin (STZ, 180 mg/kg) intraperitoneally, and blood glucose levels maintained over 350 mg/dl. Four weeks later, mice were sacrificed and ECM expression in kidney examined. Kidney cryostat sections histochemically stained with anti-fibronectin mAb, anti-collagen type IV mAb, or anti-alpha smooth muscle actin mAb (left panel, brown, 400× magnification). Bar graph shows quantification of differences in ECM expression of kidney between STZ-treated diabetic mice and untreated mice (right panel, *P < .05). b Blood and urine collected for serum creatinine and protein analyses when mice sacrificed. Level of differences in serum creatinine and proteinuria between STZ-treated diabetic mice and untreated mice (*P < .05). c MDSC ratios (CD11b⁺/Gr-1⁺) in BM, blood, spleen, and kidneys of STZ-treated diabetic mice and untreated mice compared. Isolated cells were two-color stained with specific mAbs against CD11b and Gr-1 for flow analyses. Double-positive CD11b and Gr-1 cells represent MDSCs (*P < .05). d Cryostat sections of spleen and kidney from STZ-treated diabetic mice and untreated mice double-stained with anti-CD11b (green) and anti-Gr-1 (red) mAbs and evaluated under fluorescent microscope (400× magnification; upper panel). Double-positive cells counted. In total, 10 high-power fields randomly selected in each section. Data expressed as mean CD11b⁺/Gr-1⁺ cells ± 1 SD (lower panel, *P < .05). Data representative of three separate experiments. α-SMA alpha-smooth muscle actin, ECM extracellular matrix, MDSC myeloid-derived suppressor cell