Effects of Smoking Cessation on Gene Expression in Human Leukocytes of Chronic Smoker.
- Author:
Soo Jeong KIM
1
;
Su Young KIM
;
Jae Hwa KIM
;
Dai Jin KIM
Author Information
1. Department of Psychiatry, Seoul St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Republic of Korea. kdj922@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Nicotine cessation;
Microarray;
Leucocytes;
Real time PCR
- MeSH:
Biomarkers;
Biological Processes;
Cell Adhesion;
Cytoskeleton;
Gene Expression*;
Humans;
Leukocytes*;
Microarray Analysis;
Mortality;
Peptides;
Real-Time Polymerase Chain Reaction;
RNA, Messenger;
Smoking;
Smoking Cessation*;
Tropomodulin;
Ubiquitin
- From:Psychiatry Investigation
2014;11(3):290-296
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: The risks of cigarette smoking concerning higher systemic disease mortality are lessened by smoking cessation. METHODS: Microarray analysis compared the expression profiles of smokers who were successful and not successful at smoking cessation, with the goal of identifying genes that might serve as potential biomarkers or that might be valuable in elucidating distinct biological mechanisms. The mRNAs were isolated and compared from peripheral leukocytes of six smokers who were successful in cessation and six smokers who failed in smoking cessation. RESULTS: Two hundred ninety nine genes displayed significantly different expression; 196 genes were up-regulated and 103 genes were down-regulated in the success group compared to the failure group. Twenty four of these genes were identified with biological processes including immunity, cytoskeleton and cell growth/cycle. Real-time PCR confirmed the differential gene expression. The mRNA levels of HEPACAM family member 2 (HEPACAM2) and tropomodulin 1 (TMOD1) were significantly more expressed in the success group, while the mRNA ubiquitin specific peptides 18 (USP18) were significantly less expressed in the success group compared to the failure group. CONCLUSION: The results suggest that smoking cessation can modulate cell adhesion and immune response by regulating expression levels of genes, especially HEPACAM2, TMOD1 and USP18, which have an important relationship with smoking cessation.
