[A study on expression of Wnt signal pathway gene in familial aggregated hypertension].

OBJECTIVE: To determine the role of gene expression of Wnt signal pathway in the pathogenesis of familial aggregated hypertension. METHODS: The patients having directly related family members for more than three generations suffering from hypertension were enlisted in the hypertension group, and healthy individuals served as control group. The real-time polymerase chain reaction (PCR) gene array was used to detect the expression of functional classification genes of Wnt signal pathway in peripheral blood, with standard value deviated>2.0 from hypertension group/control group as differential genes. RESULTS: When hypertension group was compared with the control group, there were 6 differentially expressed genes, with 5 genes up-regulated, including Bcl-9, microphthalmia associated transcription factor (Mitf), secreted frizzled-related protein-1 (Sfrp-1), Wnt inhibiting factor-1 (Wif-1) and ribosomal protein-l13a (Rp-l13a). There was 1 gene down-regulated, i.e. dickkopf homolog-3 (Dkk-3). CONCLUSION: The result of this study suggested that the Wnt signal pathway may be related to the occurrence and development of the familial aggregated hypertension.

[Study on cardiovascular diseases marker gene expression profile of familial aggregation hypertension].

OBJECTIVE: To explore the cardiovascular diseases marker gene expression profile of the familial aggregation hypertension patients,and to screen differentially expressed genes. METHODS: The patients who had directly related family members for more than three generations suffering from hypertension were selected as experiment group, and healthy individuals as control group. Oligo GEArray gene chip technique was used to detect the expression of cardiovascular diseases marker gene in peripheral blood. The ratio of positive/negative standard value >2.0, or ≤0.5 and >0 was identified as differential gene. RESULTS: Compared with control group, there were 10 up-regulated differential genes in experiment group, composing genes involved in lipid metabolism, immune response-related molecules, cell adhesion molecules, extracellular molecules and coagulation, including apolipoprotein E (ApoE), epithelial V-like antigen-1 (EVA-1), interferon-γ (IFN-γ), interleukin-1ß (IL-1ß), IL-8, integrin-ß1 (ITGB-1), matrix metalloproteinase-9 (MMP-9), nuclear factor-ΚB (NF-ΚB), platelet endothelial cell adhesion molecule-1 (PECAM-1), selectin-P (SEL-P). There were 3 down-regulated genes, including coagulation factors-III (F-III), lectin-like oxidized low density lipoprotein receptor-1 (LOX-1), and serine protease inhibitor-1 (SERPINE-1). CONCLUSION: This study suggested that familial aggregation hypertension related to a variety of gene markers of cardiovascular disease, especially elements concerning coagulation and extracellular protease inhibitor-related genes.

[Association of endothelial nitric oxide synthase gene polymorphism with level of uric acid in serum for acute coronary syndrome].

OBJECTIVE: To evaluate the association of elevation in serum uric acid with the development of coronary artery disease, and to determine the relationship between uric acid and Glu(298) Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene in acute coronary syndrome (ACS) in the Chinese Han Nationality. METHODS: The Glu(298) Asp variant of the eNOS gene was detected by polymerase chain reaction/restriction fragment length polymorphism analysis in 58 patients with ACS and 43 healthy controls. The severity of ACS was expressed by the number of affected vessels and by the Duke scoring system. RESULTS: The frequencies of the eNOS Glu/Glu, Glu/Asp, and Asp/Asp genotypes in the ACS group were not significantly different from those of controls (43.1%, 36.2%, 20.7% vs. 48.8%, 34.9%, 16.3%, respectively; chi (2) = 0.446, P = 0.800). In comparison with subjects who had Glu(298) allele in the eNOS gene, the risk of ACS was not increased among Asp/Asp carriers (odds ratio 1.34, 95% confidence interval 0.479 to 3.755, P = 0.575). There was no significant association between the eNOS Glu(298) Asp variant and the Duke score [(46.73+/-19.90) score for Asp/Asp vs. (48.33+/-19.61) score and (38.19+/-15.12) score for Glu/Glu and Glu/Asp, respectively, P=0.248], but there was a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level in ACS group [(298.92+/-87.27) micromol/L for Glu/Glu vs.(380.80+/-95.80) micromol/L and (346.16+/-93.71) micromol/L for Glu/Asp and Asp/Asp, respectively, P = 0.017]. CONCLUSION: Glu(298) Asp polymorphism of the eNOS gene appears to have no association with ACS in the Chinese Han Nationality, but a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level is found in patients with ACS.