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Pitavastatin Reduces Inflammation in Atherosclerotic Plaques in Apolipoprotein
E-Deficient Mice with Late Stage Renal Disease
#MMPMID26367531
Shibasaki M
; Wang JG
; Figueiredo JL
; New SE
; Quillard T
; Goettsch C
; Koga J
; Sonoki H
; Matsumoto J
; Aikawa M
; Aikawa E
PLoS One
2015[]; 10
(9
): e0138047
PMID26367531
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OBJECTIVES: Chronic renal disease (CRD) accelerates atherosclerosis and
cardiovascular calcification. Statins reduce low-density lipoprotein-cholesterol
levels in patients with CRD, however, the benefits of statins on cardiovascular
disease in CRD remain unclear. This study has determined the effects of
pitavastatin, the newest statin, on arterial inflammation and calcification in
atherogenic mice with CRD. METHODS AND RESULTS: CRD was induced by 5/6
nephrectomy in cholesterol-fed apolipoprotein E-deficient mice. Mice were
randomized into three groups: control mice, CRD mice, and CRD mice treated with
pitavastatin. Ultrasonography showed that pitavastatin treatment significantly
attenuated luminal stenosis in brachiocephalic arteries of CRD mice.
Near-infrared molecular imaging and correlative Mac3 immunostaining demonstrated
a significant reduction in macrophage accumulation in pitavastatin-treated CRD
mice. Pitavastatin treatment reduced levels of osteopontin in plasma and
atherosclerotic lesions in CRD mice, but did not produce a significant reduction
in calcification in atherosclerotic plaques as assesses by histology. CRD mice
had significantly higher levels of phosphate in plasma than did control mice,
which did not change by pitavastatin. In vitro, pitavastatin suppressed the
expression of osteopontin in peritoneal macrophages stimulated with phosphate or
calcium/phosphate in concentrations similar to those found in human patients with
CRD. CONCLUSION: Our study provides in vivo evidence that pitavastatin reduces
inflammation within atherosclerotic lesions in CRD mice.
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