1. Pitavastatin-induced downregulation of CCR2 and CCR5 in monocytes is associated with the arrest of cell-cycle in S phase 
Masahiro Fujino, Shin-ichiro Miura, Yoshino Matsuo, Hiroaki Tanigawa, Akira Kawamura, Keijiro Saku 
Atherosclerosis 
Volume 187, Issue 2, Pages (August 2006)
DOI: /j.atherosclerosis
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

2. Fig. 1
(a) Number of cells by lipophilic statin (pitavastatin) and hydrophobic statin (pravastatin) for up to 48h under serum conditions using a hematocytometer (n=3, mean±S.D.). *p<0.05 vs. no treatment. (b) Proliferative effects of pitavastatin after 24h under serum conditions as assessed by MTS assay (n=3). p<0.05 vs. no treatment. Graph shows the inhibition of proliferation as a percentage of proliferation with no treatment (n=3, mean±S.D.). *p<0.05 vs. no treatment.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

3. Fig. 2
Cell-cycle analysis with treatment with or without pitavastatin and pravastatin for 24h under serum-free conditions. The cell-cycle stage was assessed by a flow cytometric analysis (n=3, mean±S.E.). *p<0.05 vs. no treatment.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

4. Fig. 3
Representative CCR2 and CCR5 expression with treatment with or without pitavastatin in U937 cells assessed by flow cytometric analysis is shown in (a). U937 cells were treated with or without pitavastatin or pravastatin for 24h under serum-free conditions, and then CCR2 and CCR5 expression was analyzed (n=3, mean±S.D.). (b) Graph shows as a percentage of inhibition of CCR2- or CCR5-positive cells compared to no treatment (n=3, mean±S.D.). *p<0.05 vs. no treatment.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

5. Fig. 4
Proliferative effects of treatment with or without pitavastatin in addition to lower concentrations of RANTES or MCP-1 for 24h under serum-free conditions using a hematocytometer (a) or MTS assay (c). In CCR2 and CCR5 transfection experiments, CCR2 and CCR5 cDNA was transfected to U937 cells, and high expression levels of CCR2 (CCR2 positive cells: n=3, 93±6%) and CCR5 (CCR5 positive cells: n=3, 32±5%) was found as assessed by flow cytometry (b) at 24h after transfection. Proliferative effects of treatment with pitavastatin in addition to lower concentrations of RANTES and/or MCP-1 for additional 24h under serum-free conditions were analyzed using a MTS assay (b). The Y-axis indicates the inhibition of proliferation as a percentage of proliferation with no treatment (n=3, mean±S.D.). *p<0.05. NS, not significant.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

6. Fig. 5
The expression levels of p21waf1, p27kip1, cdk4, cyclin D1 and β-actin treated with or without RANTES or MCP-1 in the presence or absence of pitavastatin by immunoblotting for 24h under serum-free conditions. Three independent experiments showed similar results. Pictures show representative immunoblotting results.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions

7. Fig. 6
Proposed mechanisms of the anti-proliferative effect of pitavastatin through chemokines as a pleiotropic effect for anti-atherosclerosis in monocytes.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2005 Elsevier Ireland Ltd Terms and Conditions