Clinical Research On Association Of CD36Single Nucleotide Polymorphisms With Essential Hypertension

Background：Essential hypertension is a prevalent disorder that affects20to30%of the population worldwideand contributes significantly to mortality and morbidity from cerebrovascular disease, myocardialinfarction, congestive heart failure and renal insufficiency. Korkor et al used whole blood as asurrogate tissue for gene expression in patients with essential hypertension and identified49differentially expressed genes, among which CD36was up-regulated. Then we wondered: Is CD36acandidate gene for EH? Nowadays, there are few studies referring to the question. Therefore, wecarried out the present study to try to find the satisfying answer to the question.Objectives：1. Genotyping the CD36gene polymorphisms in Chinese Han population residing in JilinProvince；2. To investigate the genotypic and allelic distributions of CD36in Chinese Han populationresiding in Jilin Province and determine the associations of the CD36gene polymorphisms with EH；3. To explore the relationship between the CD36gene polymorphisms and individual componentof EH.Subjects and MethodsIn this study, we recruited272subjects with essential hypertension(EH) and317age-andsex-matched normal subjects without diabetes mellitus. Height, weight, body mass index(BMI),systolic blood pressure(SBP), diasolic blood pressure(DBP), high density lipoprotein cholesterol(HDL-c), low density lipoprotein cholesterol (LDL-c), fasting blood glucose (FBG), triglyceride(TG), total cholesterol(TC), blood urea nitrogen (BUN), serum creatinine (SCr) were measured. TheCD36polymorphisms were detected using direct sequending and restriction fragment lengthpolymorphism-polymerase chain reaction(RFLP-PCR) or single strand conformation polymorphism-polymerase chain reaction(SSCP-PCR). The relationship between CD36SNPs and EH wasdetermined.Results1. Clinical characteristics of the EH group and the control group: There were no significantdifferences in age, sex, height, weight, BMI, HDL-c, TC(P>0.05). Compared with control group, HR,LDL-c, TG, FBG, BUN(all of them: P<0.01) and SBP, DBP, MAP, SCr(all of them P<0.05) were significantly higher in EH group.2.The results of PCR sequending: We randomly selected100DNA samples including50from MSgroup and50from controls to detect the sequence of intron4, exon7and exon13by directsequencing method.+216T/C，+273A/G，+132C/T，+217T/C，+212T/G and+233T/C were identified,and they were consistent with the SNP labeled rs3211938, rs10499859, rs75326924, rs1953298,rs7789369and rs1527479in the National Center for Biotechnology Information(NCBI) database.3ofthe6SNPs,+273A/G,+217T/C and+212T/G were further evaluated.3. Comparison among genotypes of+273A/G①Comparison of clinical charactics among genotypers of+273A/G in EH group and controls：inEH group, compared with those with AA genotypes, HDL-c in patients with GG was significantlyhigher(P<0.05); in controls, compared with those with AA genotypers, BUN in patients with GA wassignificantly lower(P<0.05); Other clinical charactics showed no significant differences amonggenotypers. Meanwhile, in control group, no significant differences of clinical charactics wereobserved(P>0.05).②The distribution of genotypic frequencies of+273A/G showed significant difference betweenEH and controls, and G allelic frequencies were higher in EH(P<0.05).4. Comparison among genotypes of+233T/C①Comparison of clinical charactics among genotypes of+233T/C in EH group and controls: inEH group, compared with those with TT genotypers, HR in patients with CC was significantlylower(P<0.05); in controls, compared with those with TT genotypers, SBP, DBP in patients with CCwas significantly lower(P<0.05); other clinical charactics showed no significant differences amonggenotypes.②The distribution of genotypic frequencies of+233T/C showed no significant difference betweenEH and controls.5.Comparison among genotypes of+212T/G①Comparison of clinical charactics among genotypes of+212T/G in EH group and controls：inEH group, compared with those with TT genotypers, HR in patients with GG was significantlyhigher(P<0.01); in controls, compared with those with TT genotypers, SBP, DBP, MAP in patientswith TG was significantly lower(P<0.05); other clinical charactics showed no significant differencesamong genotypers. Meanwhile, in control group, no significant differences of clinical charactics wereobserved(P>0.05).②The distribution of genotypic frequencies of+212T/G showed no significant difference betweenEH and controls (P>0.05).6. CD36SNPs and EH Distributions of genotypes AA, GA and GG of+273A/G were significantly different(EH:AA58%, GA36%, GG16%, the controls: AA70%, GA25%, GG5%, χ2is10.578, P<0.01). Comparedwith the controls, G allele was significantly higher(P<0.01, OR=1.629,95%CI[1.224-2.168]),indicating that+273G allele was the significant predictor of hypertension.Conclusions1. The gene of CD36polymorphisms including+273A/G,+217T/C,+212T/G and+233T/C inintron4,+132C/T in exon7and+216T/C in exon13were identified in Chinese Han populationresiding in Jilin Province.2. The distributions of genotypic frequencies of+273A/G showed significant difference betweenEH and controls, indicating that+273A/G polymorphism was associated with the susceptibility to EH.However, the distributions of+212T/G and+233T/C genotypic and allelic frequencies were notsignificantly different.3. CD36+273G was an independent predictor of EH.