Expression of dioxin-responsive genes in human endometrial cells in culture.
To investigate expression of dioxin-responsive genes in human endometrial cells with exposure to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), human endometrial stromal cells immortalized with temperature-sensitive SV40 T antigen were used for the experiments. Cells were treated with 0.1% DMSO or 0.1, 1, 10, or 100 nM TCDD for 24 h. Induction of interleukin-1beta (IL-1beta) and plasminogen activator inhibitor-2 (PAI-2) mRNAs was analyzed by reverse-transcription polymerase chain reaction. Expression of IL-1beta or PAI-2 mRNA in response to TCDD was increased in a dose-dependent fashion. The maximum increases of PAI-2 and IL-1beta mRNAs were observed at 100 and 10 nM TCDD, respectively. While cycloheximide treatment did not show a significant difference of PAI-2 mRNA levels between control and TCDD-treated cells, mRNA stability assay using actinomycin D showed that PAI-2 mRNA in TCDD-treated cells was about twofold more stable than the control cells. While expression of CYP1A1 mRNA was not detected and levels of ARNT mRNA were not altered by TCDD exposure, the amount of AhR mRNA was decreased dose dependently. The present study represents an initial attempt to determine the responses of dioxin-responsive genes in human endometrial cells following TCDD exposure. The results demonstrated that IL-1beta and PAI-2 genes are induced dose dependently in human endometrial cells with exposure to TCDD and expression of PAI-2 mRNA is controlled at the posttranscriptional level.
Yang
J H
JH
School of Medicine, Catholic University of Taegu-Hyosung, Taegu, Republic of Korea. yangjh@cuth.cataegu.ac.kr
D051784:Aryl Hydrocarbon Receptor Nuclear Translocator; D002461:Cell Line, Transformed; D003513:Cycloheximide / Q000494:pharmacology; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics; D004268:DNA-Binding Proteins; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004717:Endometrium / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D005796:Genes; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D017396:Plasminogen Activator Inhibitor 2 / Q000235:genetics*; D000072317:Polychlorinated Dibenzodioxins / Q000494:pharmacology*; D012323:RNA Processing, Post-Transcriptional / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017154:Stromal Cells; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics
C497396:ARNT protein, human; D004268:DNA-Binding Proteins; D007375:Interleukin-1; D017396:Plasminogen Activator Inhibitor 2; D000072317:Polychlorinated Dibenzodioxins; D012333:RNA, Messenger; D018336:Receptors, Aryl Hydrocarbon; D014157:Transcription Factors; D051784:Aryl Hydrocarbon Receptor Nuclear Translocator; D003609:Dactinomycin; D003513:Cycloheximide; D019363:Cytochrome P-450 CYP1A1