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2018 ; 18
(1
): 87-96
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Lysophosphatidic acid enhances neointimal hyperplasia following vascular injury
through modulating proliferation, autophagy, inflammation and oxidative stress
#MMPMID29749484
Shen X
; Zou J
; Li F
; Zhang T
; Guo T
Mol Med Rep
2018[Jul]; 18
(1
): 87-96
PMID29749484
show ga
Lysophosphatidic acid (LPA), which is one of the intermediate products of
membrane phospholipid metabolism, is a bioactive phospholipid that possesses
diverse activities. In the present study, the effects of LPA on neointimal
formation following vascular injury were investigated. A carotid artery balloon
injury model was employed in the present study, and following vascular injury,
rats received an intraperitoneal injection of 1 mg/kg LPA. Subsequently,
histopathological alterations were assessed by hematoxylin and eosin staining,
the expression levels of proliferating cell nuclear antigen (PCNA) were detected
by immunohistochemistry, apoptosis was assessed via a terminal deoxynucleotidyl
transferase?mediated dUTP nick end labeling assay, and the expression levels of
apoptosis?associated and autophagy?associated proteins were detected by western
blotting. In addition, inflammatory and oxidative stress?associated factors were
assessed by reverse transcription?quantitative polymerase chain reaction or
corresponding kits. The results of the present study demonstrated that LPA
enhanced vascular injury?induced neointimal hyperplasia. LPA further elevated the
expression levels of PCNA in the injured carotid artery tissues. LPA exhibited no
effect on apoptosis in carotid artery tissues, whereas it modulated autophagy in
the injured carotid artery tissues. Furthermore, LPA enhanced vascular
injury?induced inflammation and oxidative stress. The present study demonstrated
that LPA may enhance neointimal hyperplasia following vascular injury by
modulating proliferation, autophagy, inflammation and oxidative stress, but not
apoptosis. Furthermore LPA may contribute to the pathology of atherosclerosis and
may be considered a promising therapeutic target for the treatment of
atherosclerosis.