Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/33027
Title: Estrogen receptor-alpha and -beta expression in microvascular endothelial cells and smooth muscle cells of myometrium and leiomyoma.
Authors: Rogers P.A.W.;Gargett C.E.;Bucak K.;Zaitseva M.;Chu S.;Taylor N.;Fuller P.J.
Institution: (Gargett, Bucak, Zaitseva, Taylor, Rogers) Monash University, Department of Obstetrics and Gynaecology, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia (Chu, Fuller) Prince Henry's Institute of Medical Research, 246 Clayton Road, Clayton, Vic. 3186, Australia
Issue Date: 18-Oct-2012
Copyright year: 2002
Publisher: Oxford University Press (Great Clarendon Street, Oxford OX2 6DP, United Kingdom)
Place of publication: United Kingdom
Publication information: Molecular Human Reproduction. 8 (8) (pp 770-775), 2002. Date of Publication: 2002.
Abstract: The two estrogen receptors, ERalpha and ERbeta, are likely to have roles in the pathophysiology of fibroid development. They have been detected in myometrial and leiomyoma (fibroid) tissue, but the cell types expressing ERalpha and ERbeta have not been determined. ERs have also been detected in human endothelial cells. The aims of the present study were to determine whether pure populations of myometrial microvascular endothelial cells (MEC) express ERalpha and ERbeta, to compare MEC ERalpha/ERbeta expression with that of pure populations of myometrial smooth muscle cells (SMC) and to determine if ERalpha/ERbeta are differentially expressed in MEC and SMC of myometrium and fibroids from nine paired samples. Using RT-PCR (for ERalpha and ERbeta) and Western blotting (for ERalpha only), we demonstrated that all cultures of early passage myometrial and fibroid SMC (>99% pure) expressed ERalpha but not ERbeta, while myometrial and fibroid MEC (>99% CD31+) constitutively expressed ERbeta. However, both myometrial and fibroid MEC showed variable expression of ERalpha, with ~60% of MEC samples expressing ERalpha. While the majority (6/9) of MEC from myometrial and fibroid pairs demonstrated the same pattern of ERalpha expression, 3/9 pairs showed discordant ERalpha expression. These results show that ERalpha and ERbeta are differentially expressed in SMC and MEC of human myometrium and fibroids. Since ERalpha and ERbeta mediate opposing transcriptional activities, any effect of estrogen on the growth and development of fibroids is likely to be complex and may involve both SMC and MEC.
PubMed URL: 12149410 [http://www.ncbi.nlm.nih.gov/pubmed/?term=12149410]
ISSN: 1360-9947
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/33027
Type: Article
Subjects: genetic transcription
adult
article
cell culture
cell population
cell type
controlled study
endothelium cell
female
human
human cell
human tissue
*leiomyoma/et [Etiology]
microvascularization
*myometrium
pathophysiology
priority journal
protein expression
reverse transcription polymerase chain reaction
smooth muscle fiber
tissue growth
*uterus myoma/et [Etiology]
Western blotting
estrogen/ec [Endogenous Compound]
*estrogen receptor alpha/ec [Endogenous Compound]
*estrogen receptor beta/ec [Endogenous Compound]
controlled study
endothelium cell
female
genetic transcription
human
human cell
human tissue
*leiomyoma / *etiology
microvascularization
*myometrium
pathophysiology
priority journal
protein expression
reverse transcription polymerase chain reaction
Western blotting
tissue growth
smooth muscle fiber
adult
article
cell culture
cell population
cell type
*uterus myoma / *etiology
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