ABSTRACT
Recurrent spontaneous abortion (RSA) is an important disease affecting female reproductive health, with an incidence of 1%-5%. The causes of RSA are complex, among which genetic factor is one of the common causes. A large number of studies in recent years have shown that RSA is closely related to the polymorphism of related genes. Normal fetal development requires the successful implantation of embryos and the maintenance of pregnancy, in which the maternal immune system and blood system play an important regulatory role. Therefore, the present paper summarized the relationship of the genetic polymorphism of maternal immune system and blood system to RSA, aiming to elucidate the pathogenesis of RSA at the gene level and provide accurate and feasible guidance for clinical prevention and treatment of RSA.
ABSTRACT
This study was aimed to investigate the anti-angiogenesis of IFN-alpha2b in chronic myeloid leukemia (CML) in vitro by using K562 cell line and human umbilical vein endothelial cells (HUVEC). The levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in culture supernatant of K562 cells were determined by ELISA; the expressions of VEGF and bFGF mRNA after treating K562 cells with 10(3), 10(2) and 10 U/ml IFN-alpha2b for 24, 36, 48 hours were detected by real-time RT-PCR; the effects of K562 cell culture supernatant and IFN-alpha2b on proliferation, migration and differentiation of HUVEC in vitro were assayed by MTT, Transwell chamber and tubule formation assay respectively. The results showed that the K562 cells expressed and secreted VEGF and bFGF. The culture supernatant of K562 cells significantly promoted the proliferation, migration and tubule formation of HUVEC in vitro in a concentration-dependent manner. After treating K562 cells with IFN-alpha2b 10 U/ml for 24, 36 and 48 hours, the expression levels of VEGF and bFGF mRNA were 1.64+/-0.18, 1.49+/-0.14, 1.31+/-0.05 and 1.53+/-0.10, 1.29+/-0.15, 0.79+/-0.13 respectively (p=0.002), but the expression levels of VEGF and bFGF mRNA were not significantly different along with increasing of IFN-alpha2b concentration. It is concluded that the angiogenesis exists in CML. The K562 cell expresses and secrets VEGF and bFGF, which promotes the proliferation, migration and differentiation of HUVEC. The IFN-alpha2b displays anti-angiogenesis by inhibiting the proliferation, migration and tubule formation in vitro of HUVEC and down regulating the expression of VEGF and bFGF mRNA.