The process of DNA methylation usually occurs at the CpG sites and the methyl group to the 5' position of a cytosine in a CpG dinucleotide conferred by DNA meth-

����� ��������� �� ��� ���� ������ ���� �� ��� ���matory and immune disease, and the prevalence and incidence of gout increases annually. Genetic variations in the DNA methyltransferases (DNMTs) gene have not, to the best of our k��wl�dg�, b��� �������d �� �������� g��� �x�������� ��d �� participate in the pathogenesis of gout. The aim of the present study was to investigate whether the DNMT1, DNMT3A and DNMT3B polymorphisms contribute to gout susceptibility. These polymorphisms were screened for in 336 gout patients and 306 healthy control subjects (from a South China population) for association with gout. The distribution frequencies of DNMT1 rs2228611 AA genotype (P=0.007) and A allele (P=0.002; odds ratio=1.508, 95% confidence �����v�l=1.158�1.964) w��� ����d �� b� ��g��fi����l� ��������d in the gout patients when compared with those in the healthy control subjects. The rs1550117 in DNMT3A and rs2424913 in DNMT3B �x��b���d �� ��g��fi���� ������������ w��� g��� susceptibility between the patients and control subjects. These results demonstrated that the DNMT1 rs2228611 polymorphism may be involved in the pathogenesis of gout, while DNMT3A rs1550117 and DNMT3B rs2424913 did not show any obvious ��g��fi����� �� ��� ������� ���d�; ����, ��� ��� b� ���d �� ���k factors to predict the susceptibility to gout. However, further studies are required to investigate the functions and regulatory mechanism of the polymorphisms of DNMTs in gout. Introduction ���� ��������� �� ��� ���� ������ ����������� ��d ������ disease affecting 1-2% of adults worldwide, which is associated with elevated serum urate levels and the deposition of monosodium urate (MSU) in the joints (1). Previous studies show that gout is also associated with the genetic background, a purine rich diet and alcohol consumption (2-4), and epidemiological studies have suggested that the prevalence and incidence of gout are increasing globally (5,6). Over the past decade, signif����� �������fi� �dv����� ��v� b��� ��d� �� ��d������d��g ��� �����g������ ��d ��������� �� g���. B���g � ����l�x d������, ��� �d����fi������ �� g������ ��d ��v���������l ���k ������� ��� gout may facilitate with investigating the pathogenesis of gout. As with other diseases, epigenetic events or heritable changes �� g��� �x�������� �������� w������ DNA ��q����� �l��������� may be evaluated to gain insight into the concrete pathogenesis of gout (7). DNA methylation is the most common epigenetic ��d�fi������, ��d �� ��������� �� ������������� ��d ��� ����matin structure (8). The process of DNA methylation usually occurs at the CpG sites and the methyl group to the 5' position of a cytosine in a CpG dinucleotide conferred by DNA methyltransferases (DNMTs) (9). Three primary DNMTs, DNMT1, DNMT3A ��d DNMT3B, ��� �������� gl�b�l DNA ����ylation (10). In addition, DNMT1 is a primary enzyme for maintaining methylation patterns during DNA replication, whereas DNMT3A and DNMT3B act predominantly as the de novo methyltransferases, and create novel methylation patterns (11-13). In addition, DNA methylation and its regulatory enzymes have been implicated in a diverse set of biological processes, including X chromosome inactivation, genomic imprinting, as well as autoimmunity (14-17). Mutation of the human DNMTs �l���� g��� �x�������� ��d ��� ���v�d� ����g�� ���� ��� �����nism of various diseases, such as centromere instability, acute ���l��d l��k���� ��d ������d�fi������ (18�20). T��������, it DNMTs may be important in the pathogenesis of autoimmune diseases. The single nucleotide polymorphism (SNP) 14463G>C of the DNMT1 gene was demonstrated to be associated with higher lupus disease activity (21). And Nam et al (22) Association of DNA methyltransferase polymorphisms with susceptibility to primary gouty arthritis XIAOWU ZHONG1-3*, YUANHONG PENG4*, CHENGJIAO YAO2*, YUFENG QING4, QIBIN YANG4, XIAOLAN GUO1,3, WENGUANG XIE1,2, MINGCAI ZHAO1-3, XIAOMING CAI5 and JING-GUO ZHOU3,4 1Department of Clinical Laboratory and 2M�d����� R������� C�����, A�fil����d H������l �� N���� S������ M�d���l C�ll�g�, Nanchong, Sichuan 637000; 3Department of Laboratory Medicine, North Sichuan Medical College, Nanchong, Sichuan 637007; 4D��������� �� R�������l�g� ��d I�����l�g� �� ��� A�fil����d H������l, North Sichuan Medical College, Nanchong, Sichuan 637000; 5Department of Biology, North Sichuan Medical College, Nanchong, Sichuan 637007, P.R. China Received April 13, 2016; Accepted July 27, 2016 DOI: 10.3892/br.2016.746 Correspondence to: Professor Jing-Guo Zhou, Department of Rheumatology and Immunology of the Affiliated Hospital, North Sichuan Medical College, 63 Wenhua Road, Nanchong, Sichuan 637000, P.R. China E-mail: [email protected] *Contributed equally