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Mol. Cells 2012; 34(5): 457-461

Published online November 30, 2012

https://doi.org/10.1007/s10059-012-0205-0

© The Korean Society for Molecular and Cellular Biology

Nicotine Induces the Expression of C-Reactive Protein via MAPK-Dependent Signal Pathway in U937 Macrophages

Junjun Mao1,2, Juntian Liu1,*, Xiaoming Pang1, Ming Li3, Jinyan Song1, Chunjie Han4, Di Wu1, and Shuyue Wang1

1Department of Pharmacology, Xi’an Jiaotong University School of Medicine, Xi’an, P.R. China, 2Department of Pharmacy, the Affiliated Hospital of Xi’an Medical College, Xi’an, P.R. China, 3Department of Pharmacy, Lianyungang Hospital of Traditional Chinese Medicine, Lianyungang, China, 4Department of Pharmacology, Shaanxi Institute for Food and Drug Control, Xi’an, P.R. China

Correspondence to : *Correspondence: ljt@mail.xjtu.edu.cn

Received: August 13, 2012; Revised: September 26, 2012; Accepted: September 28, 2012

Abstract

Atherosclerosis is an inflammatory disease in the vessel wall. Nicotine, a major component of cigarette smoke, is an independent risk factor for cardiovascular diseases including atherosclerosis. As an inflammatory molecule, C- reactive protein (CRP) participates in atherogenesis. Although it has been confirmed that CRP level in smoking patient is significantly higher than non-smokers and cigarette withdrawal,it is unknown whether nicotine induces CRP expression in macrophages. The present study was to observe effect of nicotine on CRP production and the related signal pathway in U937 macrophages. The results showed that nicotine significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent ways. Nicotinic acetylcholine receptor (nAChR) blocker hexamethonium, MEK1/2 inhibitor PD98059, p38 MAPK inhibitor SB203580 and NF-?B inhibitor PDTC almost completely abolished nicotine-induced CRP expression in mRNA and protein levels in U937 macrophages. The further study indicated that hexa-methonium, PD98059, and SB203580 significantly inhibited ERK1/2 and p38 MAPK phosphorylation. These demonstrate that nicotine has ability to induce CRP ex-pression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-?B signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers.

Keywords atherosclerosis, C-reactive protein, inflammation, macrophages, nicotine

Article

Research Article

Mol. Cells 2012; 34(5): 457-461

Published online November 30, 2012 https://doi.org/10.1007/s10059-012-0205-0

Copyright © The Korean Society for Molecular and Cellular Biology.

Nicotine Induces the Expression of C-Reactive Protein via MAPK-Dependent Signal Pathway in U937 Macrophages

Junjun Mao1,2, Juntian Liu1,*, Xiaoming Pang1, Ming Li3, Jinyan Song1, Chunjie Han4, Di Wu1, and Shuyue Wang1

1Department of Pharmacology, Xi’an Jiaotong University School of Medicine, Xi’an, P.R. China, 2Department of Pharmacy, the Affiliated Hospital of Xi’an Medical College, Xi’an, P.R. China, 3Department of Pharmacy, Lianyungang Hospital of Traditional Chinese Medicine, Lianyungang, China, 4Department of Pharmacology, Shaanxi Institute for Food and Drug Control, Xi’an, P.R. China

Correspondence to:*Correspondence: ljt@mail.xjtu.edu.cn

Received: August 13, 2012; Revised: September 26, 2012; Accepted: September 28, 2012

Abstract

Atherosclerosis is an inflammatory disease in the vessel wall. Nicotine, a major component of cigarette smoke, is an independent risk factor for cardiovascular diseases including atherosclerosis. As an inflammatory molecule, C- reactive protein (CRP) participates in atherogenesis. Although it has been confirmed that CRP level in smoking patient is significantly higher than non-smokers and cigarette withdrawal,it is unknown whether nicotine induces CRP expression in macrophages. The present study was to observe effect of nicotine on CRP production and the related signal pathway in U937 macrophages. The results showed that nicotine significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent ways. Nicotinic acetylcholine receptor (nAChR) blocker hexamethonium, MEK1/2 inhibitor PD98059, p38 MAPK inhibitor SB203580 and NF-?B inhibitor PDTC almost completely abolished nicotine-induced CRP expression in mRNA and protein levels in U937 macrophages. The further study indicated that hexa-methonium, PD98059, and SB203580 significantly inhibited ERK1/2 and p38 MAPK phosphorylation. These demonstrate that nicotine has ability to induce CRP ex-pression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-?B signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers.

Keywords: atherosclerosis, C-reactive protein, inflammation, macrophages, nicotine

Mol. Cells
Jan 31, 2023 Vol.46 No.1, pp. 1~67
COVER PICTURE
RNAs form diverse shapes and play multiple functions as central molecules of gene expression. In this special issue on RNA, seven minireviews illustrate how basic concepts and recent RNA biology findings are transformed into new and exciting RNA therapeutics.

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