| Objective:Mast cells have been implicated in the pathogenesis of coronary atherosclerosis heart disease. They can be activated by immunoglobulin E (IgE)-mediated mechanisms to release powerful mediators affecting local blood flow. Previous studies have indicated that CMAl promoter polymorphism rs1800875may be involved in regulating immunoglobulin E (IgE) levels in patients with eczema, and it is associated with the progression of immunoglobulin A nephropathy. So, the gene of mast cell chymase(CMA1) is an ideal candidate for investigating the genetic predisposition to coronary heart disease (CAD).Methods:A total of270patients underwent coronary angiography in the2nd affiliated hospital, Zhejiang University College of Medicine were enrolled. Of them,175CAD subjects was CAD group and95non-CAD subjects was control group. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was employed to detect the single nucleotide polymorphism (SNP) of rs1800875; Enzyme-linked immunosorbnent assay (ELISA) was used to measure the serum chymase and immunoglobulin E. The association between SNP rs1800875, serum chymase, and serum IgE levels was examined.Results:There was no significant difference in allele frequency between CAD and non-CAD. However, a significant association was found between CMA1genotypes and total IgE levels in CAD subjects. Meanwhile, crossover analysis revealed that, in GG homozygotes, CHD risk was nearly six times higher in those with IgE (IU/ml) level <2.58(natural logarithm conversion), while no association was found with chymase level.Conclusions:Polymorphism rs1800875of CMA1may be associated with serum IgE level in CAD subjects, but not with chymase level in both groups. In GG homozygotes, high IgE level is a protective factor against coronary disease. |