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2016 ; 12
(7
): 812-23
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Transient Receptor Potential Ankyrin 1 Channel Involved in Atherosclerosis and
Macrophage-Foam Cell Formation
#MMPMID27313495
Zhao JF
; Shyue SK
; Kou YR
; Lu TM
; Lee TS
Int J Biol Sci
2016[]; 12
(7
): 812-23
PMID27313495
show ga
Transient receptor potential ankyrin 1 channel (TRPA1) plays an important role in
the pathogenesis of inflammatory diseases, yet its role and the underlying
mechanism in atherosclerosis remain unclear. We aimed to investigate the role of
TRPA1 in atherosclerosis and foam-cell formation in vivo in mice and in vitro in
mouse macrophages. Histopathology was examined by hematoxylin and eosin staining,
levels of cytokines and lipid profile were evaluated by assay kits, and protein
expression was determined by western blot analysis. TRPA1 expression was
increased in macrophage foam cells in atherosclerotic aortas of apolipoprotein
E-deficient (apoE(-/-)) mice. Atherosclerotic lesions, hyperlipidemia and
systemic inflammation were worsened with chronic administration of the TRPA1
channel antagonist HC030031 or genetic ablation of TRPA1 (TRPA1(-/-)) in
apoE(-/-) mice. Treatment with allyl isothiocyanate (AITC, a TRPA1 agonist)
retarded the progression of atherosclerosis in apoE(-/-) mice but not
apoE(-/-)TRPA1(-/-) mice. Mouse macrophages showed oxidized low-density
lipoprotein (oxLDL) activated TRPA1 channels. OxLDL-induced lipid accumulation of
macrophages was exacerbated by HC030031 or loss of function of TRPA1. Inhibition
of TRPA1 activity did not alter oxLDL internalization but impaired cholesterol
efflux by downregulating the ATP-binding cassette transporters. Furthermore,
tumor necrosis factor-?-induced inflammatory response was attenuated in
AITC-activated macrophages. TRPA1 may be a pivotal regulator in the pathogenesis
of atherosclerosis and cholesterol metabolism of macrophage foam cells.
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