[The heat shock protein 70-2 gene +1267(A/G) polymorphism and susceptibility to ankylosing spondylitis in Chinese Han population].

OBJECTIVE: To investigate the association between the heat shock protein 70-2 gene polymorphism and ankylosing spondylitis (AS). METHODS: The polymorphisms of HSP70-2 gene Pst I 1267 site were analysed in 176 Chinese Han AS patients and 127 healthy controls by PCR and restriction fragment length polymorphisms(RFLP) methods. RESULTS: In AS patients HSP70-2 genotypes AA, AG and GG were 46.6%, 46.0% and 7.4% respectively, frequencies of A and G were 69.6%(A) and 30.4%(G). In healthy controls HSP70-2 genotypes AA, AG and GG were 44.1%, 48.8% and 6.9% respectively, frequencies of A and G were 68.5%(A)and 31.5%(G). No significant differences were found in the distribution of HSP70-2 genotypes and allele frequencies between AS patients and controls. CONCLUSION: Our results indicate that the there may be no association of the HSP70-2 gene polymorphism with AS in Chinese Han population.

[Relationship between heat shock protein 70-hom gene polymorphism and ankylosing spondylitis].

OBJECTIVE: To investigate the association between heat shock protein 70-hom (HSP70-hom) gene polymorphism and ankylosing spondylitis(AS) in Chinese Han patients. METHODS: Genomic DNA from 98 Chinese AS patients and 70 ethnically matched controls were typed for HSP70-hom polymorphism by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The HSP70-hom genotypes in the AS patients consisted of homozygote AA (60.2%) and BB(4.1%), and heterozygote(35.7%), while the HSP70-hom genotypes in the controls were composed of AA(58.6%), BB(2.9%) and heterozygote(38.6%). No significant difference was found in the distribution of HSP70-hom genotype between these two groups(chi(2) test=0.280, P>0.05). The frequencies of HSP70-hom alleles in AS patients were 77.9%(AA) and 22.1%(BB), while they were 78.1% and 21.9% in the controls. The frequency of HSP70-hom allele in AS patients was not significantly increased, compared with that in controls (chi(2) test=0.002, P>0.05). CONCLUSION: There may be no association between the HSP70-hom gene polymorphism and ankylosing spondylitis in Chinese Han population.

[Anti-apoptosis effect of VEGF on the human chronic myelocytic leukemia cell line K562].

To explore the effects of vascular endothelial growth factor (VEGF) on the mechanisms of CML pathogenesis, the effect of VEGF on K562 cell apoptosis induced by As(2)O(3) was analyzed through morphologic observation, DNA fragmentation agarose gel electrophoresis and DNA ploidy flow cytometry analysis, and the effect of VEGF on the expression of bcl-X(L), Bax and caspase-3 in K562 cells was determined by Western blot, meanwhile the expression difference between bcl-X(L) and Bax mRNA in above conditions was detected by RT-PCR. The results showed that after VEGF added, the apoptosis of K562 cells reduced, however, there was no significant changes in cell cycle distribution (P > 0.05). At the same time, following the increasing of the concentration of VEGF, expression of mRNA and protein of bcl-X(L) was up-regulated and the expression of Bax protein was down-regulated in K562 cells, and the activation of pro-caspase-3 into caspase-3 was inhibited or reduced. It is concluded that VEGF may suppress the apoptosis of K562 cells through its influence on the bcl-X(L)/Bax expression ratio in K562 cells.

[Inhibition of K562 cell proliferation by wild type p16 and p53 genes co-transfection].

The tumor suppressor gene p53 and p16, both of which play an important role in inhibition of tumorigenesis, are homozygously deleted in human myeloid leukemia cell line K562. To explore the inhibition of K562 cell proliferation by wild type p16 and p53 genes, both p16 and p53 genes were co-transfected into K562 cells mediated by liposome. The expression of the two genes was measured by immunocytochemical method, the cell cycle was analysed by flow cytometry, and the number of recovered viable cells was assessed after transfection. After co-transfection, the p53 and p16 positive cells were 23% and 28%, respectively. The results showed that co-transfection of p16 and p53 genes significantly inhibits cell proliferation comparing with transfection either by p16 gene or by p53 gene (P < 0.05). Expression of p16 and p53 proteins increased the cell number in G(1) phase but decreased the cell number in S phase. It is concluded that co-transfection of p16 and p53 genes has a stronger growth-inhibitory effect on K562 cell growth than that of transfection only by p16 gene or by p53 gene, may be a pathway for gene therapy in leukemia.