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2016 ; 13
(6
): 5021-8
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P?selectin increases angiotensin II?induced cardiac inflammation and fibrosis via
platelet activation
#MMPMID27121797
Liu G
; Liang B
; Song X
; Bai R
; Qin W
; Sun X
; Lu Y
; Bian Y
; Xiao C
Mol Med Rep
2016[Jun]; 13
(6
): 5021-8
PMID27121797
show ga
Platelet activation is important in hypertension?induced cardiac inflammation and
fibrosis. P-selectin expression significantly (P<0.05) increases when platelets
are activated during hypertension. Although P?selectin recruits leukocytes to
sites of inflammation, the role of P?selectin in cardiac inflammation and
fibrosis remains to be elucidated. The present study aimed to investigate whether
platelet?derived P?selectin promotes hypertensive cardiac inflammation and
fibrosis. P?selectin knockout (P?sel KO) mice and wild?type (WT) C57BL/6
littermates were infused with angiotensin II (Ang II) at 1,500 ng/kg/min for
7 days and then cross?transplanted with platelets originating from either WT or
P?sel KO mice. P?selectin expression was increased in the myocardium and plasma
of hypertensive mice, and the P?sel KO mice exhibited significantly (P<0.05)
reduced cardiac fibrosis. The fibrotic areas were markedly smaller in the hearts
of P?sel KO mice compared with WT mice, as assessed by Masson's trichrome
staining. In addition, ??smooth muscle actin and transforming growth factor ?1
(TGF??1) expression levels were decreased in the P?sel KO mice, as assessed by
immunohistochemistry. Following platelet transplantation into P?sel KO mice, the
number of Mac?2 (galectin?3)? and TGF??1?positive cells was increased in mice
that received WT platelets compared with those that received P?sel KO platelets,
and the mRNA expression levels of collagen I and TGF??1 were also increased. The
results from the present study suggest that activated platelets secrete
P?selectin to promote cardiac inflammation and fibrosis in Ang II?induced
hypertension.