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Cited by 213Estrogen and related hormone effectsSteroid Chemistry and BiochemistryAdrenal Hormones and Disorders

17 beta-Hydroxysteroid dehydrogenase type 2: chromosomal assignment and progestin regulation of gene expression in human endometrium.

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Casey, M L, MacDonald, P C, Andersson, S·1994·Journal of Clinical Investigation
DOI 10.1172/jci117569PMC PMC294662
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Abstract

The cDNAs for two separate human 17 beta-hydroxysteroid dehydrogenases (17 beta-HSD) have been isolated and sequenced. The well-studied human placental cytosolic 17 beta-HSD (also referred to as estradiol dehydrogenase) preferentially catalyzes the reduction of estrone to estradiol-17 beta and the reduction of the C-20-ketone of progesterone to 20 alpha-dihydroprogesterone. This isoform of the enzyme has been referred to as 17 beta-HSD type 1 and localized to chromosome 17. A second 17 beta-HSD isoform (referred to as type 2) is localized in the endoplasmic reticulum of human trophoblast and is characterized by the preferential oxidation of the C-17 beta-hydroxyl group of C18- and C19-steroids and the C-20 alpha-hydroxyl group of 20 alpha-dihydroprogesterone. In this study, we determined the chromosomal localization of human 17 beta-HSD type 2, the expression of this gene in human endometrium, and the tissue distribution of the mRNA. We found that the human 17 beta-HSD type 2 gene is localized on chromosome 16, 16q24. 17 beta-HSD type 2 mRNA (approximately 1.5 kb) was identified in human endometrial tissues by Northern analysis of total RNA (10 micrograms). The highest levels of 17 beta-HSD type 2 mRNA were found in endometrial tissues obtained during the mid- to late secretory phase of the ovarian cycle (i.e., during the time of high plasma levels of progesterone). 17 beta-HSD type 2 mRNA levels were much greater in glandular epithelium than in the stromal cells isolated from secretory phase endometrium. The levels of 17 beta-HSD type 2 mRNA in secretory phase endometrium were approximately one-tenth that in villous trophoblast tissue from human placenta. We did not detect 17 beta-HSD type 1 mRNA in endometrial tissue by Northern analysis of total (10 micrograms) RNA. These findings are consistent with the view that the progestin-regulated 17 beta-HSD of the glandular epithelium of the human endometrium is primarily, if not exclusively, the product of the 17 beta-HSD type 2 gene. 17 beta-HSD type 2 mRNA was present in human placenta, liver, and small intestine; much smaller amounts, barely detectable by Northern analysis of poly(A)+ RNA, were present in prostate, kidney, pancreas, and colon, but not in heart, brain, skeletal muscle, spleen, thymus, ovary, or testis.

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  • Progesterone via PGR induces retinoic acid production in endometrial stromal cells, which then acts on epithelial cells to induce HSD17B2 expression.

    “Progesterone via PGR induces retinoic acid production in endometrial stromal cells, which then acts on epithelial cells to induce HSD17B2 expression”

    From Endometriosis and nuclear receptors (2019) · cites this paper as Casey et al., 1994

    The Discussion (page not available) identifies HSD17B2 as a progestin-responsive gene in endometrial glandular epithelial cells and says its mRNA increases as progesterone secretion rises. The paper does not establish the claimed mechanism involving PGR-dependent retinoic acid production in stromal cells or its action on epithelial cells; searches for retinoic acid and PGR found no supporting passage. (LLM, conf=0.88)

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  • A cDNA encoding microsomal HSD17B2 was cloned and found to be expressed in endometrium, placenta, and other tissues.

    “Instead, a cDNA encoding microsomal HSD17B2 was cloned (513) and found to be expressed in endometrium, placenta, and other tissues (514).”

    From The Molecular Biology, Biochemistry, and Physiology of Human Steroidogenesis and Its Disorders (2011) · cites this paper as [514]

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Research works printed but not linked: 1

  1. [4]4. Baird, D. T. 1976. Content and secretion of steroids by the human ovary in vivo. In Proceedings of the Fifth International Congress of Endocrinology. vol

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Authors
Casey, M. L., MacDonald, P. C., & Andersson, S.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1994-11-01
Volume
94
Issue
5
Pages
2135-2141
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci117569
PMC
PMC294662
OpenAlex
W2053311013
Semantic Scholar
e0c45caf9b177e26120a97b0a2082feb33ac7b43
Cited by
212
References
46
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 6 · 2018: 9 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 3
FWCI
5.90
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50hd011149-17)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (5-P50-HD-11149)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Steroid Chemistry and Biochemistry
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
chromosomal localization, endometrium, luteal phase, progesterone regulation, gene expression, trophoblast, endoplasmic reticulum, glandular epithelium, stromal cells
MeSH terms
Chromosome Mapping, Chromosomes, Human, Pair 16, Endometrium, Female, Gene Expression Regulation, Humans, Isoenzymes, Placenta, Progestins, RNA, Messenger, 17-Hydroxysteroid Dehydrogenases

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