Oxidative
low-density lipoprotein (ox-LDL)-induced
endothelial cell injury is a key contributor toatherosclerosis development. However, the
role and mechanism of
long noncoding RNA X-inactive specifictranscript (XIST) in
atherosclerosis remain largely unknown. The ox-LDL-induced
human umbilical veinendothelial
cells (HUVECs)
injury was analyzed by
cell viability,
apoptosis, inflammatory cytokines secretionand
oxidative stress. The expression levels of XIST,
microRNA-204-5p (miR-204-5p) and
toll-like receptor 4(TLR4) were detected by
quantitative real-time polymerase chain reaction and
western blot, respectively. Thetarget interaction between miR-204-5p and XIST or TLR4 was explored by
bioinformatics analysis, luciferaseassay and
RNA immunoprecipitation. The expression of XIST was enhanced in ox-LDL-treatedHUVECs. Knockdown of XIST attenuated ox-LDL-induced viability inhibition,
apoptosis production,inflammatory response and
oxidative stress in HUVECs. XIST was validated as a
sponge of miR-204-5pand TLR4 acted as a target of miR-204-5p. Knockdown of miR-204-5p reversed silence of XISTmediated suppressive
role in ox-LDL-induced
injury. TLR4 alleviated miR-204-5p-mediated inhibitiveeffect on ox-LDL-induced
injury. Moreover, XIST could regulate TLR4 expression by spongingmiR-204-5p. In conclusion, silence of XIST displayed a protective
role in ox-LDL-induced
injury inHUVECs by regulating miR-204-5p/TLR4 axis, providing a novel mechanism for
understanding thepathogenesis of
atherosclerosis.