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. 2022 Nov 22;119(3):867–878. doi: 10.1093/cvr/cvac173

Figure 4.

Figure 4

Nicotine-induced CHI3L1/Chil1 is crucial to the augmentation of both the inflammatory response and AAA development. (A and B) Nicotine augments IL6-induced increase of CHI3L1/Chil1 gene expression in human AoSMCs and RAW264.7 cells by qRT–PCR. (C) Overexpression of miR-24 using transfection with pre-miR-24 (pre-24) reduces nicotine-augmented cytokine (IL6, CCL2 and IL8) gene expression in human AoSMCs. Scr-miR = scrambled miR control. (D–F) Nicotine augments the effects of IL6 in increasing inflammatory cytokines CCL2 (D), IL6 (E), and IL8 (F) gene expression in human AoSMCs. These effects are reduced or reversed with miR-24 overexpression (pre-miR-24 transfection). Conversely, further down-regulation of miR-24 with anti-miR-24 transfection augmented the effects on inflammatory gene expression. However, simultaneous silencing of CHI3L1 (siRNA transfection) reduces or reverses the effects of the combination of IL6, nicotine and anti-miR-24. (G) Smoking augments the increase in aortic CHI3L1 gene expression, and the decrease in miR-24 in human AAA tissue (n = 6–9 per cohort). (H) Globally induced Chil1−/− suppresses AAA growth after PPE surgery in male (left) and female mice (right) exposed to E-cig vapour for a total of 6 weeks (n = 5–13 for males; 5–10 for females). Gene expression qRT–PCR data are presented as fold change vs. control. §P < 0.05 vs. control; vs. §§ control and IL6; † vs. control, IL6, and IL6 + Nic10 nM (A–F), two-tailed student’s t-test, data are mean ± SEM (n = 3–6/treatment group). *P < 0.05 two-tailed Student’s t-test (G). Down-regulated genes are shown as −1/FC. Graphs show aortic aneurysm diameter (AAD) % increase vs. baseline. *P < 0.05 or **P < 0.01 in two-way ANOVA with multiple comparison (H).