PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25381636-6	2015	In conclusion, nicotine-induced VCAM-1, MMP-2, and MMP-9 expressions occur in a dose-dependent fashion in both of the cell lines tested.	Nicotine	15-23	vascular cell adhesion molecule 1	Mus musculus	32-38	
25381636-0	2015	Nicotine-induced upregulation of VCAM-1, MMP-2, and MMP-9 through the alpha7-nAChR-JNK pathway in RAW264.7 and MOVAS cells.	Nicotine	0-8	vascular cell adhesion molecule 1	Mus musculus	33-39	
25381636-2	2015	In the present experiment, both the RAW264.7 and MOVAS cell lines were employed to examine the nicotine-induced modulation of VCAM-1, MMP-2, and MMP-9 expressions in macrophages and vascular smooth muscle cells.	Nicotine	95-103	vascular cell adhesion molecule 1	Mus musculus	126-132	
25381636-3	2015	Our results showed that nicotine concentrations of both 0.5 and 5 ng/ml induced VCAM-1, MMP-2, and MMP-9 upregulation, while a concentration of 50 ng/ml had a slight inhibitory effect and a concentration of 500 ng/ml showed a significant inhibitory effect.	Nicotine	24-32	vascular cell adhesion molecule 1	Mus musculus	80-86	
25381636-4	2015	When cells were pretreated with either SP600125 (JNK inhibitor) or PNU-282987 (alpha7-nAChR agonist) prior to nicotine exposure, the nicotine-induced upregulation of VCAM-1, MMP-2, MMP-9, and p-JNK was suppressed, with a joint treatment producing a more significant inhibitory effect.	Nicotine	133-141	vascular cell adhesion molecule 1	Mus musculus	166-172	
25381636-7	2015	Furthermore, the nicotine exposure equivalent to plasma levels found in regular smokers can augment VCAM-1, MMP-2, and MMP-9 expressions through the alpha7-nAChR-JNK pathway.	Nicotine	17-25	vascular cell adhesion molecule 1	Mus musculus	100-106	
25803997-0	2014	Nicotine-induced ICAM-1 and VCAM-1 expression in mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway.	Nicotine	0-8	vascular cell adhesion molecule 1	Mus musculus	28-34	
25803997-2	2014	STUDY DESIGN: We determined the effect of nicotine on the expression of adhesion molecules, intercellular adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1) in mouse cardiac vascular endothelial cells and the involvement of important known intermediaries, namely p38 mitogen-activated protein kinase (MAPK) signaling pathway.	Nicotine	42-50	vascular cell adhesion molecule 1	Mus musculus	171-177	
25803997-3	2014	RESULTS: Our results indicate that nicotine can enhance the expression of ICAM-1 and VCAM-1 on mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway, resulting in increased expression of the cellular adhesion molecules ICAM-1 and VCAM-1.	Nicotine	35-43	vascular cell adhesion molecule 1	Mus musculus	85-91	
25803997-3	2014	RESULTS: Our results indicate that nicotine can enhance the expression of ICAM-1 and VCAM-1 on mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway, resulting in increased expression of the cellular adhesion molecules ICAM-1 and VCAM-1.	Nicotine	35-43	vascular cell adhesion molecule 1	Mus musculus	247-253	
25803997-4	2014	CONCLUSION: We demonstrate that 10(-6) M nicotine maximally enhances mouse cardiac vascular endothelial cell expression of ICAM-1 and VCAM-1 at 8 hours.	Nicotine	41-49	vascular cell adhesion molecule 1	Mus musculus	134-140	
21239632-4	2011	An analysis of the phenotype of isolated brain microvessels after nicotine exposure indicated higher expression of inflammatory mediators, cytokines (IL-1beta, TNF-alpha, and IL-18), chemokines (CCL2 and CX(3)CL1), and adhesion molecules (ICAM-1, VCAM-1, and P-selectins), and this was accompanied by enhanced leukocyte infiltration into brain during ischemia/reperfusion (P < 0.01).	Nicotine	66-74	vascular cell adhesion molecule 1	Mus musculus	247-253	
18472096-11	2008	Furthermore, the expression of VEGF and bFGF within CNV and VCAM-1 in choroid beneath CNV was up-regulated in nicotine-exposed mice.	Nicotine	110-118	vascular cell adhesion molecule 1	Mus musculus	60-66	
18472096-13	2008	These effects may be partly due to indirect actions of nicotine on BMCs via other factors (e.g. VEGF or VCAM-1).	Nicotine	55-63	vascular cell adhesion molecule 1	Mus musculus	104-110