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首页> 外文期刊>Molecular Biology Reports >C-reactive protein gene polymorphisms affect plasma CRP and homocysteine concentrations in subjects with and without angiographically confirmed coronary artery disease
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C-reactive protein gene polymorphisms affect plasma CRP and homocysteine concentrations in subjects with and without angiographically confirmed coronary artery disease

机译：C反应蛋白基因多态性影响有或没有血管造影证实的冠状动脉疾病的受试者的血浆CRP和高半胱氨酸浓度

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摘要

Human C-reactive protein (CRP) is a reactant involved in the acute phase response and one of the many molecular factors involved in pathogenesis of coronary artery disease (CAD). CRP gene variants potentially mediate CRP plasma concentrations and the development of CAD. 220 Croatian subjects with angiographically confirmed CAD and 132 control subjects were included in the study. CRP gene polymorphisms 1059G/C and -717G/A were determined by RFLPs, using MaeIII and KspI endonuclease, respectively. Plasma concentrations of CRP and homocysteine were determined by immunoturbidimetry and FPIA, respectively. CRP 1059G/C gene variants were significantly associated with CAD (OR = 0.50; 95% CI = 0.27, 0.94; P = 0.032). Wild GG genotype and rare allele C carrier genotypes were 184 and 22 in CAD(+) group, and 101 and 24 in CAD(−) group, respectively. Multivariate analysis with age, gender, BMI, smoking status, hypertension and diabetes as covariates showed that 1059C carriers had lower CRP concentrations in CAD(−) (P = 0.010) and CAD(+) subjects (P = 0.028). This allele was also significantly associated with lower plasma homocysteine concentrations in both groups (P = 0.018 for CAD(−) and 0.002 for CAD(+). There was no significant difference between CAD(+) and CAD(−) subjects in absolute frequencies for CRP -717A/G gene variant, but multivariate analysis showed that carriers of the rarer G allele had significantly higher CRP plasma concentrations in CAD(−) subjects (P = 0.031) and higher homocysteine concentrations in CAD(+) group (P < 0.001). Atherosclerosis is an inflammatory disease resulting from different genetic and environmental factors. Results presented here support the contribution of CRP genetic variations in the development of CAD.
机译：人C反应蛋白（CRP）是一种参与急性期反应的反应物，是参与冠心病（CAD）发病机理的许多分子因素之一。 CRP基因变异可能会介导CRP血浆浓度和CAD的发展。该研究包括220名经血管造影证实为CAD的克罗地亚受试者和132名对照受试者。通过RFLP分别使用MaeIII和KspI核酸内切酶确定CRP基因多态性1059G / C和-717G / A。分别通过免疫比浊法和FPIA测定血浆CRP和高半胱氨酸浓度。 CRP 1059G / C基因变体与CAD显着相关（OR = 0.50; 95％CI = 0.27，0.94; P = 0.032）。野生GG基因型和稀有等位基因C携带者基因型在CAD（+）组中分别为184和22，在CAD（-）组中分别为101和24。以年龄，性别，BMI，吸烟状况，高血压和糖尿病为协变量的多变量分析表明，1059C携带者的CAD（-）（P = 0.010）和CAD（+）受试者（P = 0.028）的CRP浓度较低。该等位基因还与两组血浆同型半胱氨酸浓度降低显着相关（CAD（-）P = 0.018，CAD（+）P =0.002。CAD（+）和CAD（-）受试者在绝对频率上无显着差异CRP -717A / G基因变异，但多变量分析表明，罕见的G等位基因携带者在CAD（-）受试者中具有显着更高的CRP血浆浓度（P = 0.031），在CAD（+）组中具有较高的同型半胱氨酸浓度（P < 0.001）。动脉粥样硬化是由不同的遗传和环境因素引起的炎性疾病，此处显示的结果支持了CRP基因变异在CAD发展中的贡献。

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