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. 2019 Apr 5;234(10):18731–18747. doi: 10.1002/jcp.28513

Figure 7.

Figure 7

CTRP9‐mediated downregulation of TLR4‐MyD88 protein expression is associated with AMPK phosphorylation. (a–c) TLR4 and MyD88 protein expression in the infarct border zone at Day 3 post MI with Ad‐GFP and Ad‐CTRP9 pretreatment. (d–f) Effects of TLR4 and MyD88 on macrophages treated with gCTRP9 (3 μg/ml) at different time points by western blot analysis. (g–j) Protein levels of TLR4 and MyD88 after knockdown of CTRP9 in macrophages for 24 hr. (k–m) Effects of compound C on TLR4 and MyD88 protein expression in macrophages responding to gCTRP9 via LPS + IFN‐γ stimulation using western blot analysis. Data are presented as the mean ± SEM from four independent experiments; *p < 0.05 and **p < 0.01, the connection represents a comparison between two groups. AMPK: adenosine monophosphate kinase; CTRP9: C1q/TNF‐related protein‐9; GAPDH: glyceraldehyde 3‐phosphate dehydrogenase; GFP: green fluorescent protein; IFN‐γ: interferon‐γ; LPS: lipopolysaccharide; MI: myocardial infarction; MyD88: myeloid differentiation factor 88; NF‐κB: nuclear factor‐κB; SEM: standard error of the mean; shRNA: small hairpin RNA; TLR4: toll‐like receptor 4