Identification of the regulatory regions of the human aromatase P450 (CYP19) gene involved in placenta-specific expression.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Expression of the human CYP19 gene in placental syncytiotrophoblast, ovarian granulosa and luteal cells and adipose stromal cells is regulated by tissue-specific promoters which lie upstream of unique untranslated first exons. In placenta, the majority of CYP19 mRNA transcripts contain 5'-sequences encoded by exon I.1 which lies >35 kb upstream of the translation initiation sequence in exon II. Mononuclear cytotrophoblasts isolated from midterm human placenta spontaneously fuse in culture to form multinucleated syncytiotrophoblast. These morphological changes are associated with a marked induction of CYP19 gene expression. To functionally define genomic regions required for placenta-specific expression, fusion genes containing various amounts of exon I.1 5'-flanking sequence linked to the human growth hormone (hGH) structural gene, as reporter, were introduced into human trophoblast cells in primary monolayer culture and into transgenic mice. Our findings using transfected cells and transgenic mice suggest that sequences between -501 and -42 bp upstream of exon I.1 contain a positive enhancer element(s) that mediates the actions of trophoblast-specific transcription factors, as well as a negative element(s) that binds inhibitory transcription factors in other cell types. Our findings from transgenic studies further indicate that mouse placenta contains the necessary transcripti

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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