Fig. 2: MD2 deficiency prevents diabetes-induced cardiac injury.
From: MD2 activation by direct AGE interaction drives inflammatory diabetic cardiomyopathy
Diabetes was induced in C57BL/6 wild-type and MD2−/− mice by streptozotocin. Heart tissues were harvested at 16 weeks [WT-Con = non-diabetic wild-type controls, WT-STZ = diabetic wild type, MD2KO-Con = non-diabetic MD2−/−, MD2KO-STZ = diabetic MD2−/−]. a Representative H&E staining of cardiac tissues [n = 6]. b mRNA levels of cardiac tissue Anp, Col1a1, Mmp9, Mmp2, and Tgfb1 normalized to Actb [means ± SEM; n = 6 per group; *p < 0.05, **p < 0.01, ***p < 0.001 compared with WT-Con; #p < 0.05, ##p < 0.01 compared with WT-STZ; P-values by unpaired t test are indicated]. c Representative immunoblots showing cardiac tissue ANP, Col 1, MMP-9, MMP-2, and TGF-β. GAPDH was used as a loading control [n = 6; 3 samples per group shown]. d, e Representative staining images of mouse heart sections showing Sirius Red (d) and Masson’s Trichrome (e) (n = 6 per group). f, g qPCR analysis of Tnfa and Il6 mRNA levels in cardiac tissues [means ± SEM; n = 6 per group]. h Representative immunoblots showing levels of IκB and phosphorylated ERK, JNK, and P38 in mouse cardiac tissues. GAPDH was used as loading control [n = 6; 3 samples per group shown]. Source data are provided as a Source Data file. P-values by one-way ANOVA in b, f, and g followed by Tukey’s post hoc test are indicated.
