子痫前期患者脱落滋养细胞激活血管内皮细胞的分子机制的研究

《子痫前期患者脱落滋养细胞激活血管内皮细胞的分子机制的研究》由会员上传分享，免费在线阅读，更多相关内容在学术论文-天天文库。

1、万方数据复旦大学硕士学位论文pregnanc,iesorinplacentaetreatedwithpreeclampticseraactivatedendothelialcells．TrophoblasticdebriscontainingIL-113maybeonemechanismtoinduceendotheliumactivationinpreeclampsia．2．TheroleofsyncytiotrophoblastiemicroparticlesonendothelialactivationObjectives

2、：InvestigatewhethersyncytiotrophlastmicroparticlesfromplacentaecanbephagocytoseandabsorbentbyendothelialcellsandsubsequentlymodifyingtheresponseofendothelialcellstoSTBM。Method：TodetecttheabilityofphagocytosisandclearanceofSTBM，STBMwereincubate．dwiththeconfluentmonola

3、yersofendothelialcellsfor24hours，thecellswerethenexaminedbyconfocalmicroscopyusingaLeicamodelTCSSP2confocalmicroscope．Normalfirsttrimesterplacentalexplantswereculturedindividuallywithpreeclampticornormotensivesera．thenS113Mwerecollectedandexposedtoendothelialcells．En

4、dothelialcellactivationWaSquantifiedbyceilsurfaceICAM-1．ThelevelsofIL-lpinconditionedmediumfromendothelialcellsculturedwithSTBMwerealsoquantifiedbyELISA．Results：EndothelialcellsphagocytoseSTBMandthephagocytosisofSTBMWaSsignificantlyinhibitedbycytochalsinD，aninhibitor

5、ofphagocytosis。PhagocytosisofSTBMwasincreasedinatimedependentmannerEndothelialcellbecameactivatedbythephagocytosisofSTBMfromplacentalexplantsthatWaStreatedwithpreeclampticsera，withincreasedexpressionofICAM-landreleaSingofIL-1pinconditionedmedium．Conclusion：Endothelia

6、lcellsphagocytosetrophoblastmicroparticlesfromplacentalexplants，andmicroparticlesfromplacentalexplantstreatedwithpreeclampticbutnotnormotensiveseraactivatedthephagocytosingendothelialcellsasindicatedbyincreasedICAM-1andIL．1bexpression．．Inconclusion，trophoblasticdebri

7、sextrudedfrompreeclampticplacentaactivatesendothelialcellsinanIL-1Dassociatedpathway,STBMcanbephagocytosedandabsorbentbyendothelialcellsinatimedependentmannerandSTBMfromplacentalexplantstreatedwithpreeclampticbutnotnormotensiveserainduceendothelialcellsactivation．The

8、seresultsindicatetrophoblasticdebrisisaplacentalfactorwhichinduceendothelialcelldysfunction，andmaybeusedasatherapeutictargetforpree