Skip to main content
Fig. 2 | Cardiovascular Diabetology

Fig. 2

From: Genetic deletion of MMP12 ameliorates cardiometabolic disease by improving insulin sensitivity, systemic inflammation, and atherosclerotic features in mice

Fig. 2

Reduced crown-like structure formation in DKO eWAT and downregulation of inflammatory and fibrosis-related pathways. (A) H&E staining of eWAT sections (scale bar, 100 μm). (B) mRNA expression of proinflammation genes and anti-inflammatory Adipoq in eWAT relative to Rplp0 expression (n = 6–9). (C) F4/80 immunohistochemistry in eWAT sections (scale bar, 100 μm; insets: scale bar, 50 μm). Quantification of F4/80 immunohistochemistry in eWAT sections from LdlrKO and DKO mice (n = 8 − 7) with (D) percentage of positively stained areas and (E) mean intensity in the positive areas. (F) Protein expression of BAX in eWAT. Calnexin (CNX) was used as a loading control. (G) Densitometric quantification of BAX/CNX (n = 4). (H) Volcano plot showing selected upregulated (red) and downregulated proteins (blue) reported to play a role in either inflammation and/or fibrosis in eWAT. (I) Ingenuity Pathway Analysis (IPA) from untargeted proteomics data of eWAT showing downregulated gene sets (z-score < 2 in light blue; z-score > 2 in dark blue) and upregulated gene sets (red) in DKO mice. Figures represent data from 6 LdlrKO and 6 DKO mice. Data represent mean values ± SD. *p < 0.05, **p ≤ 0.01. n.d., not detected

Back to article page