U.S. flag

An official website of the United States government

PMC Full-Text Search Results

Items: 5

2.
Fig. 2.

Fig. 2. From: The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

ABCA1 expression and its function among study groups at baseline. A: ABCA1 protein expression was suppressed in macrophages from NCAD and CAD smokers compared with those from nonsmokers (each group, n = 6). B: Densitometry (p = 0.033, p < 0.001 vs. nonsmoker). C: ABCA1 mRNA was dramatically suppressed in CAD smokers but was upregulated in macrophages from NCAD smokers compared with that from nonsmokers (p < 0.001; each group, n = 10). D: ApoA-1-mediated cholesterol efflux was decreased in macrophages from CAD smokers (p < 0.001; n = 26) and NCAD smokers (p < 0.001; n = 24) compared with those from nonsmokers (n = 10) at baseline. ApoA-1-mediated cholesterol efflux was significantly lower from CAD smokers than from NCAD smokers (p = 0.017).

Wei Song, et al. J Lipid Res. 2015 Mar;56(3):682-691.
3.
Fig. 4.

Fig. 4. From: The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

Changes of ABCA1 expression and function in macrophages from NCAD smokers after smoking cessation. A–C: ABCA1 protein expression did not change in macrophages from NCAD-smo and NCAD-abs (p = 0.458; n = 6). D: ABCA1 mRNA expression did not change in NCAD-smo and NCAD-abs (p = 0.267 and 0.089; n = 10). E: After 3 months of smoking cessation, ABCA1-mediated cholesterol efflux was increased significantly in NCAD-abs (p = 0.002; n = 12), whereas there was no change in NCAD-smo (p = 0.137; n = 12). F: The changes in ABCA1-mediated cholesterol efflux in NCAD-abs were not significantly different from those in NCAD-smo (p = 0.255).

Wei Song, et al. J Lipid Res. 2015 Mar;56(3):682-691.
4.
Fig. 5.

Fig. 5. From: The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

Inhibition of ABCA1 expression from cigarette tar in THP-1-derived macrophages. THP-1 cells were differentiated into macrophages. Macrophages were incubated in medium containing tar or nicotine for 72 h. A: ABCA1 protein expression was stimulated by 100 ng/ml nicotine, which could be reversed by BTX. C: ABCA1 protein expression was inhibited by 0.1 g/l tar, which could be abolished by LXR agonist TO901317. B and D: ABCA1 mRNA was upregulated by nicotine (p = 0.006 vs. control) and downregulated by tar (p = 0.039 vs. control). The effects of nicotine and tar on ABCA1 mRAN expression could be removed by BTX (p < 0.001 vs. nicotine) and TO901317 (p < 0.001 vs. tar), respectively.

Wei Song, et al. J Lipid Res. 2015 Mar;56(3):682-691.
5.
Fig. 3.

Fig. 3. From: The implication of cigarette smoking and cessation on macrophage cholesterol efflux in coronary artery disease patients.

Changes of ABCA1 expression and function in macrophages after smoking cessation from CAD smokers. ABCA1 protein expression did not changed in CAD-smo (p = 0.156; n = 6) (A and C), but it was increased after smoking cessation for 3 months in CAD-abs (p = 0.007; n = 6) (B and 3). D: ABCA1 mRNA expression was upregulated in macrophages from CAD-abs (p = 0.042; n = 10). E: After 3 months of smoking cessation, ABCA1-mediated cholesterol efflux was increased significantly compared with baseline in CAD-abs (p = 0.004; n = 12), whereas there was no change in CAD-smo (p = 0.473; n = 10). F: After 3 months, ABCA1-mediated cholesterol efflux increased significantly in CAD-abs compared with that in CAD-smo (p = 0.036).

Wei Song, et al. J Lipid Res. 2015 Mar;56(3):682-691.

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center