Research Paper Volume 11, Issue 19 pp 8120—8138

The interaction between STAT3 and nAChRα1 interferes with nicotine-induced atherosclerosis via Akt/mTOR signaling cascade

Figure 1. nAChRα1 mediates the nicotine-induced phosphorylation of STAT3, Akt and mTOR in MOVAS and RAW264.7 cells. (A) The effect of nAChRα1 knockdown on the protein expression and phosphorylation of ERK1/2, STAT3, Akt and mTOR in MOVAS cells (left) and RAW264.7 cells (right). (B) The opposite effect of nAChRα1 overexpression on ERK1/2, STAT3, Akt and mTOR in MOVAS cells (left) and RAW264.7 cells (right). Abbreviations: nc-si+ni, negative control siRNA plus nicotine; α1-si+nicotine, nAChRα1 siRNA plus nicotine; nc-plasmid+nicotine, negative control plasmid plus nicotine; α1-plasmid+nicotine, nAChRα1 overexpression plasmid plus nicotine. The data were presented as the mean ± SD. *p < 0.05, **p < 0.01 vs. the control group. NS, not significant vs. the control group. Each experiment was performed three times.