Knuutinen, A. et al. Smoking affects collagen synthesis and extracellular matrix turnover in human skin. Br. J. Dermatol. 146, 588-594

University of Helsinki, Helsinki, Uusimaa, Finland
British Journal of Dermatology (Impact Factor: 4.28). 05/2002; 146(4):588-94. DOI: 10.1046/j.1365-2133.2002.04694.x
Source: PubMed


Smoking is associated with premature facial wrinkling and aberrant wound healing, but the underlying mechanisms of skin injury are poorly understood.
To compare the in vivo collagen synthesis and degradation in the skin of smokers and non-smokers.
The study population consisted of 47 current smokers and 51 individuals who had never smoked from northern Finland. Suction blisters were induced in the sun-protected upper inner arm of the study subjects, after which suction blister fluid (SBF) was collected for analyses of the levels of aminoterminal procollagen propeptides of type I and III collagens (PINP and PIIINP, respectively), matrix metalloproteinase (MMP)-8 and tissue inhibitor of MMP (TIMP)-1. PINP, PIIINP and TIMP-1 were also determined from serum samples. The levels of active and pro MMP-1 were assessed from deep-frozen skin biopsies by Western blotting.
The synthesis rates of type I and III collagens were lower by 18% and 22%, respectively, in the SBF of the smokers compared with the non-smokers. The levels of MMP-8 were higher by 100% in the SBF of the smokers. The levels of MMP-1 in the skin biopsies did not differ significantly between the groups. The levels of TIMP-1 in SBF were 14% lower in the smokers than in the non-smokers, whereas the serum concentrations of TIMP-1 did not differ between the groups.
Smoking decreases the synthesis rates of type I and III collagens in skin in vivo and alters the balance of extracellular matrix turnover in skin.

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    • "On the other hand, many studies on skin and bone have shown that nicotine can cause reduction in expression of collagen types (25, 26). Also, a study on nicotine effect on collagen expression in wound scar tissue did not show any difference in expression of genes related to this protein (27). "
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    ABSTRACT: Background: Nicotine can pass through placental blood barrier and accumulate in the developing organs of fetus. Also, entering the breast milk, nicotine can have an effect on the neonates. Investigations have showed that collagen IV is one of the most important micro vessels basement membrane components. Objective: In this study, the effect of maternal nicotine exposure in pre and postnatal periods on collagen IV in microvessels of neonatal Balb/C mice brain cortex was studied by immunohistochemistry technique. Materials and Methods: 24 pregnant Balb/C mice were divided in to 4 groups (6 mice in each group): two experimental and 2 control groups. The mothers in the 1st experimental group were injected 3 mg/kg nicotine intrapritoneally from the 5th day of pregnancy to parturition daily and in 2nd experimental group the same procedure was repeated to the 10th day after parturition (lactation). The control groups received the same volume of normal saline during the same time. 10 days after delivery, the brain tissues of newborns were isolated. Then, prepared blocks from fixed brain were cut serially for immunohistochemical assay. Results: The findings of the present study indicated that collagen IV reaction in microvessels basement membrane in the first experimental group increased significantly compared to the first control group (p=0.002). In addition, collagen IV reaction in microvessels basement membrane in the 2nd experimental group increased significantly compared to the 2nd control group (p=0.002). However, no significant difference was observed between the two experimental groups. Conclusion: These results suggested that maternal nicotine exposure during prenatal period may increase basement membrane collagen IV expression. Also, nicotine increases in maternal breast milk has no effect on basement membrane collagen IV expression.
    Full-text · Article · Apr 2014 · International Journal of Reproductive BioMedicine
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    • "The association between smoking and injuries has biological plausibility, both from a physiological and psychosocial perspective. There is considerable literature showing that cigarette smoking impairs wound [53,54] and bone [55-57] healing, reduces tissue strength [58,59], and affects immune function. The immune system is important for tissue healing, since macrophages, leukocytes, and lymphocytes regulate various steps in the process and remove or assist in removal of damaged tissue [60-63], such as might be produced by repetitive microtrauma. "
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    ABSTRACT: United States Army combat engineer (ENG) training is an intense 14-week course designed to introduce new recruits to basic soldiering activities, Army values and lifestyle, and engineering skills and knowledge. The present investigation examined injury rates and injury risk factors in ENG training. At the start of their training, 1,633 male ENG recruits were administered a questionnaire containing items on date of birth, height, weight, tobacco use, prior physical activity, and injury history. Injuries during training were obtained from electronic medical records and the training units provided data on student graduation and attrition. Risk factors were identified using Cox regression. Ninety-two percent of the recruits successfully graduated from the course and 47% of the recruits experienced one or more injuries during training. Univariate Cox regression demonstrated that recruits were at higher injury risk if they reported that they were older, had a higher or lower body mass index, had smoked in the past, had performed less exercise (aerobic or muscle strength) or sports prior to ENG training, had experienced a previous time-loss lower limb injury (especially if they had not totally recovered from that injury), or had a lower educational level. The present investigation was the first to identify injury rates and identify specific factors increasing injury risk during ENG training. The identified risk factors provide a basis for recommending future prevention strategies.
    Full-text · Article · Mar 2013 · Journal of Occupational Medicine and Toxicology
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    • "Ocular hypertension causes damage to the cornea [29]. Smoking probably deteriorates ocular hypoxia caused by ocular hypertension [27], and consequently affects the biosynthesis of collagen and extracellular matrix turnover [30], which could be an explanation to the decreased corneal thickness. "
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    ABSTRACT: Background To date, studies on the role played by cigarette smoking in primary open-angle glaucoma (POAG) remains controversial. The current study evaluated cigarette smoking as a risk factor of POAG and its relationships with vertical cup-to-disc ratio (VCDR), central corneal thickness (CCT) and intraocular pressure (IOP) in a Chinese cohort. Methods In a total of 248 unrelated individuals including 30 juvenile-onset POAG (JOAG), 92 adult-onset POAG (AOAG) and 126 sex-matched senile cataract controls, underwent comprehensive ophthalmic examination. Their smoking was obtained and documented by questionnaire. Association of cigarette smoking with POAG was performed using logistic regression controlled for age and sex. Effects of cigarette smoking on VCDR, IOP and CCT were analyzed with multiple linear regression. Results In either JOAG or AOAG, no association of cigarette smoking was found with disease onset (P = 0.692 and 0.925 respectively). In controls and JOAG, no significant effects of smoking were found on VCDR, IOP or CCT (all P > 0.05). Smoking was found to be correlated with decreased CCT in AOAG and combined POAG (JOAG + AOAG) (P = 0.009 and 0.003), but no association with VCDR or IOP was observed (P > 0.05). Conclusions Although cigarette smoking was not found to be risk factor for onset of POAG, it was correlated with CCT in AOAG, and thus might still play a role in the disease course, especially for AOAG.
    Full-text · Article · Nov 2012 · BMC Ophthalmology
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