Retinoic acid and thyroid hormone regulate placental lactogen expression in human trophoblast cells.

作者: A Stephanou , S Handwerger

DOI: 10.1210/ENDO.136.3.7867602

关键词: Human placental lactogenEndocrinologyRetinoic acidReporter geneInternal medicineChloramphenicol acetyltransferaseBiologyTrophoblastTransfectionPlacental lactogenSyncytiotrophoblast

摘要: In this study, we have demonstrated that retinoic acid (RA) and thyroid hormone (T3) stimulate the synthesis release of human placental lactogen (hPL), one major secretory products syncytiotrophoblast cells. Enzymatically, dispersed trophoblast cells from term placentas exposed continuously to RA (0.5 microM) T3 (0.1 for 5 days released significantly more hPL than control after 3 exposure (P < 0.001 in each instance). On 4 5, amounts by were approximately 3- 5-fold higher those cells, respectively. The stimulation both was dose dependent accompanied messenger RNA levels. caused 3.5- 5.6-fold increases, respectively, chloramphenicol acetyltransferase activity BeWo choriocarcinoma transfected transiently with a 2.3-kilobase (kb) fragment promoter (-2300 2 basepairs) coupled reporter gene. Deletion construct analysis (2.3, 1.2, 0.5 kb) indicated T3- RA-responsive elements are localized -0.5 -1.2 kb up-stream transcriptional start site (+1), where several consensus RA- T3-responsive element sites present. These results indicate mechanism involving gene transcription further support role these steroids function.

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