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BackgroundMultiple sclerosis (MS) is an autoimmune disease that leads to myelin sheath destruction. Hypoxia‐inducible factor 1 (HIF‐1) has several roles in cells, such as inducing inflammation and angiogenesis. Recently, several lines of evidence have indicated the role of the hypoxia response and the HIF‐1 signaling pathway in an autoimmune disease such as MS. The present study aimed to evaluate the effects of HIF‐1α gene polymorphisms and vascular endothelial growth factor (VEGF) (as a major target gene of HIF‐1α) gene polymorphism on MS susceptibility.MethodsIn total, 150 MS patients and 150 healthy age‐ and gender‐matched people as a control group participated in the present study. The polymerase chain reaction‐restriction fragment length polymorphism method was used for genotyping.ResultsThe results obtained showed that the CC genotype of the VEGF rs699947 polymorphism was significantly higher in the case group than in the control group (p = 0.004). Also, we showed a significant relationship between the VEGF rs699947 polymorphism and MS in a dominant inheritance model (p = 0.005). Regarding the VEGF rs699947 polymorphism allelic distribution, the C allele frequency was significantly higher in the control group than in the case group (71.3% versus 61%, respectively, p = 0.009) and decreased the MS susceptibility by 1.6‐fold (odds ratio = 1.6, 95% confidence interval = 1.2–2.2). There was no significant difference between the two groups with respect to HIF‐1α rs11549465 genotypic distribution. The HIF‐1α C111A polymorphism was non‐polymorphic in our study population, except in the case group where nine subjects carried the CA genotype.ConclusionsWe show a significant association between VEGF rs60047 polymorphism and MS susceptibility. However, our results do not show a significant association between MS and HIF‐1α polymorphisms.

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Cigarette smoking and opium use are risk factors for coronary artery disease (CAD). It has been known that scavenger receptors such as CD36 and CD68 play critical roles in the pathogenesis of CAD. CD9, as a member of the tetraspanin, has been shown to interact with scavenger receptors. The aim of this study was to investigate the effects of these risk factors on expression levels of CD9, CD36, and CD68 on the THP-1 cell line. The THP-1 cell line treated with cigarette smoke extract (CSE( and opium, both individually and combinatory, in 24 h incubation. The protein and mRNA levels of CD9, CD36, and CD68 were evaluated by flow cytometry and quantitative reverse transcription-Polymerase Chain Reaction (qRT-PCR) techniques, respectively. CD36 and CD68 mRNA and protein expression levels were significantly increased in the cells treated with cigarette smoke extract compared to the control (p<0.001 in mRNA expression levels and p=0.016 and p=0.012 in protein expression levels, respectively). The CSE increased the level of CD9 protein expression compared to the control group (p=0.041) on the human macrophage cell line THP-1. No significant differences were observed in the CD9, CD36, and CD68 gene expression and at the protein levels between opium-treated THP-1 cells and controls. In conclusion, cigarettes by increasing the levels of CD36, CD68, and CD9 can be a risk factor in the development of many inflammatory diseases, including cardiovascular diseases, chronic obstructive pulmonary disease (COPD) and lung carcinoma.