@article {Peng:2012:1672-9145:911,
	author = "Peng, Xiaonu and Li, Wenjun and Zhang, Wei",
	title = "Poly(ADP-ribose) polymerase 1 inhibition protects human aortic endothelial cells against LPS-induced inflammation response",
	journal = "Acta Biochimica et Biophysica Sinica",
	volume = "44",
	number = "11",
	year = "2012",
	abstract = "Atherosclerosis is a chronic inflammatory disease. Toll-like receptor 4 (TLR4) is an important signaling receptor and plays a critical role in the inflammatory response. Poly(ADP-ribose) polymerase 1 (PARP1) is a nuclear enzyme that can regulate the expression of various inflammatory genes. In this study, we investigated the role and the underlying mechanisms of PARP1 on lipopolysaccharide (LPS)-induced inflammation in human aortic endothelial cells. Compared with the control, LPS stimulation increased the protein expression of TLR4 and PARP1. TLR4 inhibition reduced LPS-induced upregulation of inducible nitric oxide synthase (iNOS) and ICAM-1 as well as PARP1. Nuclear factor κB (NF-κB) inhibition decreased ICAM-1 and iNOS expression. Inhibition of PARP1 decreased protein expression of inflammatory cytokines induced by LPS stimulation, probably through preventing NF-κB nuclear translocation. Our study demonstrated that LPS increased ICAM-1 and iNOS expression via TLR4/PARP1/NF-κB pathway. PARP1 might be an indispensable factor in TLR4-mediated inflammation after LPS stimulation. PARP1 inhibition might shed light on the treatment of LPS-induced inflammatory cytokines expression during atherosclerosis.",
	pages = "911-917",
	url = "http://www.ingentaconnect.com/content/oup/abbs/2012/00000044/00000011/art00003",
	doi = "doi:10.1093/abbs/gms080",
	keyword = "human aortic endothelial cell, atherosclerosis, inflammatory cytokine, toll-like receptor 4, poly(ADP-ribose) polymerase 1, nuclear factor κB"
}