The Expression Of Connexin 43 In Gestational Trophoblastic Diseases And Its Clinical Value

Objective: There is a high incidence of gestational tmphoblast diseases (GTD) in the world. Atpreseifl, alihough the treatment of CTD is quite effecting in clinic, the paihogenesis, interrelated factors in its malignancy and pmgnosis aren't veiy clear. There have been many studies about its etiology and pathogenesis, and several hypotheses have been pmposed such as fetal prema~ death, malnuUition, viral infection, vacuous ovum feililizafion, double ova feitilizafion, et al. however there still have no one opinion. Most GTDs, which relate to pregnancy, are the diseases originating placental villous tmphoblast Villous tmphoblast originating fmm oospenn have somo genetic components as embryo somatic cells, but different from maternal somatic cells. Despite this, Trophoblast cells can invade the uterine wail and survive. Similarly, cancer cells have differential genetic components compared to non-cancer cells and can invade and survive in patients-body. Studies in cytopalhology have found that trophoblast and cancer cells have similar biologic pmperlies. There's also a similarity between the processes of their respective transformations. Therefore transformation of trophoblast into OTT would provide us a good model for the study of turnoflgenesis. Gap junctional cellular communication(GJIC) enables cells to obtain energy, signals from outside, in addition, it plays an important role in many other biological functions such as cell growth, differentiation by controlling the passage of somo irons and small molecules. Recently evidences have proved that there are abnormal expression of connexin(CX) and functional defects in GJIC among tumor and transformed cells. Expression of CX and recovery of GJIC are conelated with tumor's growth control and inhibition of transformation CX gene exhibits features of tumor suppressor genes. 5 The puipose of the research explores the re1ali~4ty of CX and GTD occuncnce and aims to pinvide a novel appmach for the therapy of GTD. Methods: With inmmunohistochemical technique and situ hybridization involving CX43 mAb and CX43 mRNA, expression of CX43 were measured in normal early pregnancy villi (6-10 wks, 20 samples), hydatidifoim rrxMe(HM) tissues of first curettage(42 samples,) tissues of invasive hydatidiform mole(IHM)(38 samples), choriocarcinoma(CC) tissues (30 samples). Result CX43 positive particles were exclusively localized in cytotnphoblast in normal early pregnancy villi. It's hardly seen anxng syncytiotmphoblast and interstitial cells. In GTDs, expression of CX43 were significantly decreased and restricted in plasma membrane. It's not expressed in nucleus and cytoplasm. There was significant difference of CX43 expression between normal human villous and GTDs(P<0.01), and there was no significant difference anmg GDs(P>0.05). Condusioir expression of CX43 is of significant difference in tix)phoblast cells between normal early pregnancy viii and abnormal pmliferated cells of GTDs. Decreased expression of CX43 and down-regulation of G.JD in tmphoblast insulted in malignant transformation Although the expression of CX43 in GTJ7s is weak than EM's, there is no significant difference between them. The reason is still unknown. We conjecture: abnormal proliferation of EM's tmphoblast cells which have some tumor properties due to the of down -regulation of CJIC.