Research Paper Volume 13, Issue 5 pp 7627—7643

Nicotine exacerbates atherosclerosis through a macrophage-mediated endothelial injury pathway

Nicotine exacerbates BMDM dysfunction by ROS production, lipid phagocytosis, and chemotaxis. (A) ROS production was measured in BMDMs by the ROS probe Relative (APC channel detected by flow cytometry), which increased with the nicotine concentrations (*P B) Lipid phagocytosis was measured in BMDMs by flow cytometry in the PE channel, which increased with nicotine concentration (*P C) chemotaxis towards medium containing CCL2 (50 ng/mL) was significantly increased in BMDMs pretreated with nicotine, as determined by a transwell assay (*P

Figure 2. Nicotine exacerbates BMDM dysfunction by ROS production, lipid phagocytosis, and chemotaxis. (A) ROS production was measured in BMDMs by the ROS probe Relative (APC channel detected by flow cytometry), which increased with the nicotine concentrations (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n=4). (B) Lipid phagocytosis was measured in BMDMs by flow cytometry in the PE channel, which increased with nicotine concentration (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n=4). (C) chemotaxis towards medium containing CCL2 (50 ng/mL) was significantly increased in BMDMs pretreated with nicotine, as determined by a transwell assay (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, n=5).