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  • Recently Zhao et al have been carried out a study

    2019-10-14

    Recently, Zhao et al. have been carried out a study to investigate the relationship between eNOS-4b/a polymorphism and the risk of LCPD in a Chinese population. Their results demonstrated that eNOS polymorphisms may be involved in the etiology of LCPD. However, the number of studies conducted to examine the eNOS polymorphism is not sufficient. Especially, there is a lack of investigation on different ethnicities. Therefore, in the present research, we hypothesize that the eNOS 27-bp VNTR, Glu298Asp andT-786C polymorphisms may have an effect on development LCPD. In order to verify the hypothesis, a case-control study was conducted to investigate the association of eNOS polymorphisms and susceptibility to LCPD in Iranian children.
    Materials and methods
    Results The general characteristics of the LCPD cases and controls are summarized in Table 1. For all participants, DNA analyses of eNOS gene polymorphisms were performed. There were no significant differences between cases and controls regarding age and gender (Table 1).
    Discussion Recently, several epidemiological studies revealed that there are various polymorphisms on eNOS gene and these mutations might be a risk factor for several diseases including Coronary artery disease, orthopedic disease and malignancies. The eNOS can produce nitric oxide (NO) from L-arginine in the endothelial cell. NO, as an important endothelium-derived factor, is synthesized in the endothelial YC 1 and plays a central role in regulating a wide spectrum of functions in the cardiovascular system, including vasorelaxation, limiting platelet aggregation, ischaemia-reperfusion injury, vascular smooth muscle cell migration and proliferation, as well as platelet aggregation., To better clarify the role of eNOS 27-bp VNTR, 894G > T and 786T > C polymorphism in LCPD risk, we conducted a case-control study. The present study involved LCPD patients with age matched healthy controls from an Iranian genetically homogenous population. Our results suggest that the two eNOS 894G > T and −786T > C polymorphisms are associated with increased risk of LCPD. The few available studies supporting this evidence include a recent study conducted by Zhao et al. in Chinese population. Regarding to the functional role of NO in regulating angiogenesis in human, it is possible that eNOS 894G > T and −786T > C polymorphisms might be positively correlated with development LCPD by affecting NO synthesis. Over the last few years several polymorphisms of the eNOS gene have been identified, and their association with orthopedic disease has been explored. Several studies revealed a statistically significant correlation of eNOS −786T > C polymorphism with neuralgia-inducing cavitational osteonecrosis, osteoporosis, idiopathic as well as secondary multifocal idiopathic osteonecrosis of the head of the femur., To the best of our knowledge this is the first study analyzing eNOS −786T > C polymorphism with LCPD. This study revealed a significantly higher percentage of homozygote mutant genotype (CC) of the eNOS −786T > C polymorphism in LCPD as compared with controls, indicating that T786C polymorphism is associated with susceptibility to LCPD patients in Iranian children. The −786T > C polymorphism in the promoter region of eNOS gene is associated with the reduction of eNOS promoter transcription rate and significantly reduced promoter activity, leading to endothelial dysfunction and reduced NO production in the vascular endothelium. It seems an impairment of NO production by eNOS −786T > C polymorphism may play in the development of LCPD. The eNOS 894G > T polymorphism, located at exon 7, leads to an amino acid substitution and subsequently leading an immature protein, in which a G > T substitution at exon 7 leads to Glu > Asp substitution at position 298. The eNOS 894G > T polymorphism can lead to low expression levels and activity of eNOS. Therefore, the TT genotype of eNOS 894G > T polymorphism caused a diminished and slower aggregation of erythrocytes, as this genotype has been shown to blunt endothelium-mediated vasodilatation and implicated as a risk factor in numerous cardiovascular conditions hypertension, coronary spasm, myocardial infarction, and coronary artery disease. We have found that the heterozygous GA genotype of eNOS 894G > T was significantly associated increased risk of LCPD (OR = 3.347, 95% CI 1.440–7.778, P = 0.005), compared with the homozygous mutant TT genotype (OR = 2.512, 95% CI 0.220–28.634, P = 0.458). Similar results for the associations of the GA genotype of eNOS 894G > T and LCPD risk were reported in a Chinese population.