Mutational analysis of β-arrestin in Japanese patients with coronary spastic angina

Coronary spastic angina （CSA） has become increasingly important for clinical practice. β-arrestin regulates a large network of cellular responses including inflammation and muscle contraction. However, little is known about its role in the pathogenesis of CSA. In this study, we performed mutational analysis of β-arrestin1 and β-arrestin2 genes in CSA patients. The study population included 20 CSA patients and 5 control subjects. Mutational analyses of the coding egions of β-arrestins were performed by direct sequencing. In β-arrestin1, single base heterozygous substitution at nucleotide position 176 in exon 5 was detected in 2 of 20 CSA patients, whereas no substitution was detected in control subjects. We subsequently performed an association study involving 50 CSA patients and 50 control subjects. No ifference was found in the incidence of the mutation between the two groups （p=0.44）. In β-arrestin2, single base substitution at nucleotide position 61 in exon 11 was detected. This substitution was homozygous in 13 and heterozygous in 7 of 20 CSA patients, whereas all homozygous in 5 control subjects. These substitutions were well-annotated SNPs rs877711 and rs1045280, respectively） and did not cause amino acid replacement. No significant substitution of the oding regions of β-arrestins was detected in Japanese CSA patients.