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ID:55684251
大小:3.56 MB
页数:6页
时间:2020-05-24
《芳香烃受体(AhR)内源性配体ITE对胎盘滋养层细胞的增殖抑制作用及其机制.pdf》由会员上传分享,免费在线阅读,更多相关内容在行业资料-天天文库。
1、复里学搪医学版FS2(¨4Jl-.41(4)488udanUnivIMedSci“’芳香烃受体(AhR)内源性配体ITE对胎盘滋养层细胞的增殖抑制作用及其机制郝克红王凯陈晓。段涛(复旦大学上海医学院研究生院}海200O32;同济大学附属匕海第一妇婴保健院转化医学中心,产科上海20004(1)【摘要】目的研究芳香烃受体(arylhydrocarbonreceptor,AhR)的内源性配体2-(1H一吲哚一3『_羰基)噻唑一4一羧酸甲酯(ITE)对胎盘滋养层细胞增殖的影响及其机制。方法用免疫组织化学及Westernblot检测AhR在早期绒毛和晚期胎盘组织中的表达,利用人胎盘滋养层细
2、胞系JEG-3和JAR作为细胞模型研究ITE对胎盘滋养层细胞增殖的影响。结果AhR主要分布于人胎盘合体滋养层细胞的胞质中,并且晚期胎盘组织中AhR蛋白的表达水平高于早期绒毛组织(P3、一3L羰基)噻唑-4-羧酸甲酯(ITE);芳香烃受体(AhR);胎盘滋养层细胞;细胞增殖;细胞周期【中图分类号】R174.1【文献标志码】Adoi:1f1.3969/j.issn.1672—8467.2014.04.011InhibitoryeffectanditsmechanismofITE,anendogenousaryihydrocarbonreceptor(AhR)ligand,ontheproliferationofhumanplacentaltrophoblastcellsHA0Ke—hong,WANGKai,CHENXiao,DUANTao△(GraduateSch4、ool,ShanghaiMedicalCollege,FudanUniversity,Shanghai2OOO32,China;ClinitalandTranslationalResearch(7enter3DepartmentofObstetrics,ShanghaiFirstMaternityandInntHospital,"gJiUniversity,Shanghai20()040。China)[Abstract]ObjectiveToinvestigatetheeffectsandmechanismof2-(1H—indole一3一carbony1)一thiazole一45、一carboxylieacidmethylester(ITE),anendogenousarylhydrocarbonreceptor(AhR)ligand,ontheproliferationofhumanplacentaltrophoblastcelllines.MethodsWeexaminedtheproteinexpressioninthefirsttrimesterandtermhumanplacentasusingimmunohistochemistryandWesternblot.Thenweusedhumanplacentalchoriocarcinomaeel6、llinesJEG-3andJARascellmodelstoinvestigatetheeffectsofITEontheirproliferation.ResultsAhRwasmainlypresentedintheACorrespondingauthorE—mail:tduan@yahoo.corn郝克红,等.芳香烃受体(AhR)内源性配体ITE对胎盘滋养层细胞的增殖抑制作用及其机制489cytoplasmofsyncytiotrophob1asts,andtheproteinlevelsofAhRintermplacentaswassignificantlyincrea7、sedascomparedwiththeirlevelsinthefirsttrimesterplacentas(P<0.()5).TheproteinlevelsofAhRinJEG-3weremuchhigherthanitslevelsinJAR.ITEtime—anddose—dependentlyinducedCytochromeP4501A1(CYP1A1)mRNAexpressioninJE3cell,butnotJARcel1.Importantly,ITEsig
3、一3L羰基)噻唑-4-羧酸甲酯(ITE);芳香烃受体(AhR);胎盘滋养层细胞;细胞增殖;细胞周期【中图分类号】R174.1【文献标志码】Adoi:1f1.3969/j.issn.1672—8467.2014.04.011InhibitoryeffectanditsmechanismofITE,anendogenousaryihydrocarbonreceptor(AhR)ligand,ontheproliferationofhumanplacentaltrophoblastcellsHA0Ke—hong,WANGKai,CHENXiao,DUANTao△(GraduateSch
4、ool,ShanghaiMedicalCollege,FudanUniversity,Shanghai2OOO32,China;ClinitalandTranslationalResearch(7enter3DepartmentofObstetrics,ShanghaiFirstMaternityandInntHospital,"gJiUniversity,Shanghai20()040。China)[Abstract]ObjectiveToinvestigatetheeffectsandmechanismof2-(1H—indole一3一carbony1)一thiazole一4
5、一carboxylieacidmethylester(ITE),anendogenousarylhydrocarbonreceptor(AhR)ligand,ontheproliferationofhumanplacentaltrophoblastcelllines.MethodsWeexaminedtheproteinexpressioninthefirsttrimesterandtermhumanplacentasusingimmunohistochemistryandWesternblot.Thenweusedhumanplacentalchoriocarcinomaeel
6、llinesJEG-3andJARascellmodelstoinvestigatetheeffectsofITEontheirproliferation.ResultsAhRwasmainlypresentedintheACorrespondingauthorE—mail:tduan@yahoo.corn郝克红,等.芳香烃受体(AhR)内源性配体ITE对胎盘滋养层细胞的增殖抑制作用及其机制489cytoplasmofsyncytiotrophob1asts,andtheproteinlevelsofAhRintermplacentaswassignificantlyincrea
7、sedascomparedwiththeirlevelsinthefirsttrimesterplacentas(P<0.()5).TheproteinlevelsofAhRinJEG-3weremuchhigherthanitslevelsinJAR.ITEtime—anddose—dependentlyinducedCytochromeP4501A1(CYP1A1)mRNAexpressioninJE3cell,butnotJARcel1.Importantly,ITEsig
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