| Hypertensive disorder complicating pregnancy,a specific sydrome tohumans gestation,is a triad of edema ,hypertension and proteinuria disappearingafter delivery and remains a major cause of maternal and perinatal mortality andmorbility.Pathogenesis of hypertensive disorder complicating pregnancy isunknown that is the reason of hypertensive disorder complicating pregnancy as adisease of theories,which include superficial implantation.Many rearchers notedthat uterine muscle strench ischemia and immune tolerance in maternal andplacenta interference can lead to impeded spiral arteries remodeling,compromised placental perfusion and trophoblast ischemia ,Which associatewith superficial implantation.Placenta formation rely on differentiation of epithelial cells and cytotrophoblasts.Trophoblast invasion is regulated by a balanced interplay betweentrophoblasts and decidual cells or/and vascular endothelial cells .Which causeendometrium and vascular remodeling.Rearches show that remodeling of spiralatteries is limited to decidual level in hypertensive disorder complicatingpregnancy.Which has been proved that 30%-50% spiral arteries is not beeninvaded by trophoblasts.That is the reason of insurfficient placental perfusi-on.Which can cause hypertensive disorder complicating pregnancy.MMPs,belonging to the proteases family,have the function to decidual matrixbasal memberances and vascular walls.in order to facilitate trophoblastsinvasion. EMMPRIN is one of member of immunoglobin superfamily ,and takepart in placenta growth ,embryo implantation and regulating endothelial cells.Ithas been proved that EMMPRIN and MMPs exist in normal tissue as well askinds of tumors.MMPs play a role in stromal ECM remodeling and neova-scularisation in decidualization to benefit implatation.EMMPRIN canup-regulate MMPs to increase MMPs products.as MMPs up-regulator.EMMPRIN and MMPs existing in endormetrium cells ,decidual cells andtrophoblasts cells.attend embryo implatation and placenta angiogenesis.Theassociation of MMPs with normal and complicated pregency has been rearchedgenerally.MMPs is key factors to implantation and vascular rebuilding.Howevere,reports on EMMPRIN are limited ,except the relationship ofEMMPRIN and normal.There is still no related reports on EMMPRIN andhypertensive disorder complicating pregnancy .So,in this research,We study the expression of EMMPRIN and MMP-1,MMP-2 in placentas of pre-eclampsia.in order to explore their fuction andmechanism in hypertensive disorder complicating pregnancy.Methods:Immunohistochemsitry (SABC) was used to determine the distribution andintensity of MMP-1,MMP-2 and EMMPRIN staining in placentas of 36 casesof pre-eclampsia (12 of mild and severe cases respective and 12 cases ofeclampsia ) and 12 cases of non-complicated pregnancy.Then,groups werecompared with each other by statistics methord.Results:1.Microscope results show malnutrious villous decreased humbers ofvasculars,blood clot and fibronecrosis in vasulars.2.Expression character:MMP-1,MMP-2 and EMMPRIN expressed introphoblasts, vascular endothelial cells and chorionic matrix.MMP-1andMMP-2 existed mainly in decidual cells,matrix cells and trophoblasts.EMMPRIN expressed in decidual cytotrophoblasts in common and in decidualmatrix occasionally.3.The expression of MMP-1,MMP-2 was significantly decreased ingroup. Compared with the normal group(P<0.05).And the expression wasdecreased with progress of pre-eclampsia (P>0.05).There were no significantdifferential between pre-eclanpsia and eclampsia group.4.The expression of EMMPRIN was significantly decreased in group.Compared with the normal group(P<0.05).And the expression was decreasedwith progress of pre-eclampsia (P>0.05).There were no significant differentialbetween pre-eclanpsia and eclampsia group.Conclusions:(1)MMP-1,MMP-2 and EMMPRIN expressed in tropgoblasts , vascularendothelial cells and chorionic matrix.(2)MMP-1,MMP-2 and EMMPRIN were decreased with the progress ofhypertensive disorder complicating pregnancy.except for severe preeclampsiaand eclampsia,because there is no obviouse deffer -ence between them.(3)The decreased expression of MMP-1,MMP-2 and EMMPRIN inplacenta leads to insufficient trophoblasts infiltration and might be one of thepathogengsis of pre-eclampsia and eclampsia.(4)MMP-1,MMP-2 and EMMPRIN maybe have correlations with eachother. |