Galectin-3 gene (LGALS3) +292C allele is a genetic predisposition factor for rheumatoid arthritis in Taiwan

• Published in: Clinical rheumatology 2011-09, Vol.30 (9), p.1227-1233
• Main Authors: Hu, Chung-Yi, Chang, Sheng-Kai, Wu, Chien-Sheng, Tsai, Wei-I, Hsu, Ping-Ning
• Format: Article
• Language: English
• Subjects: Apoptosis; Arthritis, Rheumatoid - ethnology; Arthritis, Rheumatoid - genetics; Female; Galectin 3 - genetics; galectin-3; Gene Frequency; Gene polymorphism; Genetic Predisposition to Disease; Humans; Inflammation; Lectins; Male; Medicine; Medicine & Public Health; Middle Aged; Nucleic Acid Hybridization; Oligonucleotide Probes; Oligonucleotides; Original Article; Polymerase chain reaction; Polymorphism, Restriction Fragment Length; Polymorphism, Single Nucleotide; Probes; Restriction fragment length polymorphism; Rheumatoid arthritis; Rheumatoid synovitis; Rheumatology; Single-nucleotide polymorphism; Taiwan - epidemiology
• ISSN: 0770-3198; 1434-9949
• DOI: 10.1007/s10067-011-1741-2

Galectin-3 is a beta-galactoside-binding lectin which is involved in modulating inflammation and apoptosis. Elevated expression of galectin-3 has been demonstrated in synovium of rheumatoid arthritis (RA). The aim of our study is to investigate the genetic polymorphisms of galectin-3 in association with RA. Polymorphisms of galectin-3 gene ( LGALS3 ) were compared between 151 RA patients and 182 healthy subjects in Taiwan. Variants at two LGALS3 single nucleotide polymorphism (SNP) sites (rs4644 and rs4652, corresponding to LAGLS3 +191 and +292) were genotyped by polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) and sequence-specific oligonucleotide probe hybridization, respectively. The allelic carriage of LGALS3 +292C was increased in patients with RA (66.9% in RA vs. 52.7% in controls, odds ratio = 1.8, 95% confidence interval = 1.2–2.8, p  = 0.009). These results implicate that the genetic polymorphisms in galectin-3 gene may contribute to development of RA.