[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.

[Evaluation of in vivo labeled cytotoxic T lymphocytes and cytokine-induced killer cells migration and distribution of subcutaneous gastric tumor model in nude mice].

OBJECTIVE: To investigate the migration and distribution of CTL (cytotoxic T lymphocyte) and CIK (cytokine-induced killer) cells in gastric tumor model. METHODS: Subcutaneous gastric tumor model was established by BGC-823 cancer cells in nude mice. Both CTL and CIK cells were labeled with 99Tc(m) directly and then inoculated into nude mice with subcutaneous tumor by intravenous injection separately. Three mice of each group were evaluated by single-photon emission computerized tomography (SPECT) at 1 h, 6 h and 24 h post-inoculation. After SPECT imaging, 3 mice in each group were sacrificed and got samples of the tumor, liver, spleen, kidney, lung, intestine, etc. The tissue samples were weighed and radioactivity was determined with a well-type scintillation counter. The accumulation of labeled CTL and CIK cells in tissues were expressed as %ID/g (percentage activity of injection dose per gram of tissue) and T/NT (tumor/non-tumor) values were analyzed. RESULTS: The tracing of both cells in SPECT showed a clear migration path away from the injection point to solid tumor, and can be detected in all organs and tissues such as liver, spleen, kidney, lung and intestine, etc not long after injection. The %ID/g peak values of CTL in organs from the highest to the lowest were as follows: tumor (7.79 +/- 0.46), liver (4.12 +/- 0.51), intestine (2.71 +/- 0.16), kidney (1.44 +/- 0.25), spleen (1.24 +/- 0.12), kidney (1.12 +/- 0.11), and all the T/NTs were above 1. The %ID/g peak values of CIK cells in organs from the highest to the lowest were as follows: liver (6.64 +/- 0.67), tumor (5.47 +/- 0.87), intestine (3.55 +/- 0.23), kidney (2.34 +/- 0.41), spleen (1.45 +/- 0.17), lung (1.27 +/- 0.21), and T/NTs > 1 except for liver. After injection, the %ID/g values of tumor in CTL group were 2.35 +/- 0.28 (1 h), 4.58 +/- 0.52 (6 h) and 7.79 +/- 0.46 (24 h) respectively while the %ID/g values of tumor in CIK group 2.23 +/- 0.46 (1 h), 3.25 +/- 0.70 (6 h) and 5.47 +/- 0.87 (24 h) respectively. At 24 h point, the %ID/g of CTL in tumor was much higher than CIK cells (P < 0.05). CONCLUSION: The definite directional tumor-targeting capacity of CTL and CIK cells in tumor-bearing nude mice is promising.