The Effect Of Activin A On Vascular Endothelial Growth Factor And Vascular Endothelial Growth Factor Receptors In Primary Human Cytotrophoblasts In Vitro

ObjectiveVascular endothelial growth factor family, is a family of multifunctional cellfactor, and have direct an indirect adjustive function of angiogensis and lym-phangiogensis, and could promote endothelial cell proliferation, angiogensis andincreasing blood vessel permeability. Vascular endothelial growth factor in thefemale reproductive endodermis through the entire process from fertilization tobirth deliveries in the trophoblasts of the placenta and multiplication and pene-trated an important role in the development process. In early pregnancy fetal-placenta growth depends primarily on the growth of ctotrophoblast (Ctotropho-blast, CTB) division and uterine placenta of a vascular network, the existence oftwo distinct divisions CTB channels on the one hand may be a complex tropho-blasts divide (Syncytrophoblast) Executive pregnancy secretion functions; Onthe other hand experience of dividing a trophoblast invasion (Invasive Cytotroph-oblast) to parent towards education, and alternative vascular endodermis cell di-vision, uterine blood vessels and stretch fiber degradation, and the expansion ofblood vessels, decrease resistance origin, blood flow volumn increasing, geneti-cally interface vascular reconstruction. This vascular reconstruction is the gradu-al disintegration of the ctotrophoblasts type vascular endodermis cells and alter-native screw endodermis cells and small arterial blood vessels completed. Ctotro-phoblasts division and (or) bad alternative to blood vessels leading to the im-plantation of reconstruction obstacle is the failure of pregnancy and the occur-rence of certain diseases mechanism. Activin a is a member of the family TGF-β, as in adenohypophysis FSHcan stimulate the release function was separated out and surrounded by externalnaming. Recent research shows that activin, it in a variety of biological systemsplay an important role, especially in the dividing cell multiplication, and apop-tosis the functional concern. Even activin fromβmodel and divided into three dif-ferent types, namely, activin A, B and thus enlivening activin AB. Bringingquality, are widely distributed in human tissues, including placenta only activina expression. A recent study shows that heavy elements through regulation ofVEGF expression in vascular generation. Maeshima K such reports activin a per-son in vitro cultivation cattle arterial blood vessels endodermis cells (bovine aor-tic endothelial cells, BAEC) formed blood vessels, in the process marked risein the expression of VEGF and its receptors. Oppresses the antagonist follistatinusing activin A to stop the element to be possible anti-to damp the blood ves-sel production, obtains activin A to be possible to adjust VEGF the expressionthen to induce BAEC to form the blood vessel the conclusion. Whether activin Adid adjust the person ctotrophoblast to secrete VEGF, domestic and foreign stillnobody report.This experiment through establishes the person ctotrophoblast non-bloodserum raise method, determined whether control action activin A in in vitro raiseperson ctotrophoblast to the VEGF. If the study is successful, can occur fromembryos implanted with mechanisms for the "effective" to provide alternative el-ements pregnancy may be test-tube babies. On the other hand, because thereare certain disease patients placenta and thus activin a high expression of VEGFmay use this mechanism in-depth study of disease causes and to provide earlydiagnosis screening indicators, such as pregnancy hypertension disease.MethodsThis research take the normal pregnant 6-8 week-long trophoblast organ-ization as a material, raises the person ctotrophoblast with non-blood serumraise method in vitro. Immune cell chemistry confirms person ctotrophoblast ac-tivin A and VEGF and their receptors FLT-1, KDR-2 expression. RT-PCR around examination activin A function person ctotrophoblast VEGF, FLT-1,KDR-2 mRNA expression.ResultsIn vitro non-blood serum raise in human ctotrophoblast to have the VEGFand its receptors FLT-1 and the KDR-2 expression, vegf expression spotmainly concentrates in the cell membrane, next in cytoplasm; But the receptorFLT-1 expression spot mainly concentrates in the cell membrane; ReceptorKDR-2 expression in cytoplasm. VEGF and its receptors FLT-1 and the KDR-2 in stimulate the raise using activn A in the ctotrophoblasts Comparatively notto need activin A to stimulate the raise the ctotrophoblasts expression obviouslyto elevate in mRNA level.ConculsionsThe human early pregnancy ctotrophoblast expresses VEGF and its the re-ceptors. In vitro establishment has ctotrophoblast model which VEGF and its thereceptors expresses for the continuation thoroughly to discuss the embryo to im-plant certain gestation period diseases which the vascular "recast" the mecha-nism and this mechanism exceptionally causes to have the mechanism to lay thefoundation.