The Modulation of Aromatase and Estrogen Receptor Alpha in Cultured Human Dermal Papilla Cells by Dexamethasone: a Novel Mechanism for Selective Action of Estrogen Via Estrogen Receptor Beta?
From: Department of Biomedical Sciences, University of Bradford, West Yorkshire, UK. m.j.thornton@bradford.ac.uk
The Journal of investigative dermatology
- Publish Date: Sep 2006
- ISSN: 0022-202X
- Volume: 126
- Issue: 9
- Pages: 2010-8
- Medium: Print
- Language: English
- Citation (JAMA): Thornton M Julie, Nelson Louisa D, Taylor Anthony H, et al. The Modulation of Aromatase and Estrogen Receptor Alpha in Cultured Human Dermal Papilla Cells by Dexamethasone: a Novel Mechanism for Selective Action of Estrogen Via Estrogen Receptor Beta?. J. Invest. Dermatol. Sep 2006;126:2010-8
Abstract
Steroid hormones have important modulatory effects on the hair follicle, but the mechanisms by which they regulate human hair growth are still poorly understood. It is now clear that there are two distinct estrogen receptors (estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta)) that bind 17beta-estradiol. Since the follicular dermal papilla is known to control hair growth, and steroid hormones regulate receptor and aromatase expression in other tissues, we tested the hypothesis that steroid hormones would similarly modulate estrogen receptor and/or aromatase expression in cultured dermal papilla cells derived from human hair follicles. Primary cultures of non-balding occipital and frontal scalp and beard dermal papilla cells (n = 10) were established. Immunocytochemical studies showed the expression of ERalpha in both the cytoplasm and nucleus, whereas ERbeta was confined to the nuclei. The cells derived from occipital scalp were also incubated for 24 hours with 10 nM of either 17beta-estradiol, estrone, testosterone, 5alpha-dihydrotestosterone, 5alpha-androstane-3alpha, 17beta-diol, 5alpha-androstane-3beta, 17beta-diol, or 100 nM tamoxifen or dexamethasone in phenol red-free, serum-free medium to measure the steady-state levels of ERalpha, ERbeta, and aromatase mRNA by semiquantitative reverse transcriptase-PCR. Although androgens and estrogens did not alter ERalpha mRNA levels, treatment with dexamethasone significantly reduced ERalpha levels to 38% of the untreated control. By contrast, ERbeta mRNA levels were unaffected by any steroid treatment. Furthermore, dexamethasone significantly stimulated the expression of aromatase mRNA approximately 9-fold. Aromatase activity, assayed by the tritiated water method, was stimulated in both frontal scalp and beard dermal papilla cell cultures by dexamethasone. These observations provide evidence for a glucocorticoid-dependent mechanism whereby the selective action of estradiol via ERbeta may be promoted. Additionally, upregulation of aromatase combined with downregulation of ERalpha provides a basis for selective action of estradiol produced locally by autocrine or paracrine mechanisms.
Mesh Headings (Keywords): Androgens, Aromatase, Autocrine Communication, Cells, Cultured, Dermis, Dexamethasone, Estrogen Receptor alpha, Estrogen Receptor beta, Estrogens, Female, Gene Expression, Glucocorticoids, Humans, Male, Paracrine Communication, RNA, Messenger, Scalp, Up-Regulation
Check for Full Text / PubMed Unique Identifier (PMID): 16691199
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.