Inhibin and activin subunits are differentially expressed in endometrial cells and leukocytes during the menstrual cycle, in early pregnancy and in women using progestin-only contraception

Inhibins and activins are dimeric hormones which share common subunits and which have diverse endocrine and paracrine roles in regulating reproductive function. Endometrial expression of inhibin α, βA and βB subunits was examined by immunohistochemistry and in-situ hybridization, across the menstrua...

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Veröffentlicht in:Molecular human reproduction 2000-12, Vol.6 (12), p.1107-1117
Hauptverfasser: Jones, R.L., Salamonsen, L.A., Critchley, H.O.D., Rogers, P.A.W., Affandi, B., Findlay, J.K.
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Sprache:eng
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Zusammenfassung:Inhibins and activins are dimeric hormones which share common subunits and which have diverse endocrine and paracrine roles in regulating reproductive function. Endometrial expression of inhibin α, βA and βB subunits was examined by immunohistochemistry and in-situ hybridization, across the menstrual cycle and in early pregnancy. All three subunits were found to be expressed in endometrium, primarily by glandular epithelium in the early stages of the cycle. Following the onset of decidualization, expression of α, βA and βB subunits was up-regulated in decidualized stromal cells. A marked down-regulation of α subunit was detected in glandular epithelium, whilst expression of βA and βB subunits was maintained. This pattern was consistent in decidua from early pregnancy and additionally in endometrium from women using progestin-only contraceptives, either subdermal implants (Norplant®) or levonorgestrel-releasing intrauterine systems (Lng-IUS). Immunostaining was also observed for both βA and βB subunits in subpopulations of endometrial leukocytes, identified to be distinct subsets of macrophages, neutrophils and mast cells. Potential paracrine roles for activins may be envisaged in facilitating tissue remodelling during decidualization, in tissue repair following menstruation, and additionally in modulating premenstrual inflammatory events.
ISSN:1360-9947
1460-2407
1460-2407
DOI:10.1093/molehr/6.12.1107