Open AccessAn Association Study on ADAM 10 Promoter Polymorphisms and Atherosclerotic Cerebral Infarction in a Chinese Population
Author(s) -
Li You,
Liao Feng,
Yin XiaoJian,
Cui LiLi,
Ma GuoDa,
g XiaoXian,
Zhou HaiHong,
Chen YanFang,
Zhao Bin,
Li KeShen
Publication year - 2013
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12136
Subject(s) - association (psychology) , cerebral infarction , chinese population , medicine , population , genetics , biology , genotype , psychology , gene , ischemia , environmental health , psychotherapist
Summary Aim Dysregulation of the activity of the disintegrin/metalloproteinase ADAM 10 could contribute to the development of atherosclerosis. Although a number of genetic studies have focused on the association of ADAM 10 gene polymorphisms with susceptibility to diseases, no genetic association studies of ADAM 10 gene variability with atherosclerotic cerebral infarction ( ACI ) have been conducted. The aim of this study was to analyze the potential association between ADAM 10 promoter polymorphisms and ACI . Methods The associations between rs653765 and rs514049 polymorphisms of the ADAM 10 promoter and the possible risk of ACI were assessed among 347 patients with ACI and 299 matched healthy individuals in a case–control study. Results Overall, there was a significant difference in the genotypes frequencies of rs653765 ( P = 0.04) between the ACI and control subjects. In addition, the rs653765 mutated allele of ADAM 10 was significantly associated with increased ADAM 10 expression in patients with ACI ( P = 0.032). In contrast, the allele frequency of rs514049 was not statistically associated with ACI , and the rs514049 variant A > C did not affect the expression of ADAM 10 either. Conclusion Our findings indicate a positive association between the rs653765 polymorphism of ADAM 10 and ACI , as well as a negative result for rs514049. In addition, a significant increase in ADAM 10 expression was observed in patients with ACI carrying the rs653765 C > T mutation. This new knowledge about ADAM 10 might be clinically important and confirm a role for ADAM 10 in the pathophysiology of ACI , with potentially important therapeutic implications.