Format

Send to

Choose Destination
Fertil Steril. 2002 Sep;78(3):596-602.

Retinoids and steroids regulate menstrual phase histological features in human endometrial organotypic cultures.

Author information

1
Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

Abstract

OBJECTIVE:

To determine whether organotypic cultures of human endometrium can be manipulated with hormones to exhibit histological features resembling different menstrual cycle phases.

DESIGN:

Human menstrual cells were collected and cultured in monolayer and organotypic cultures.

SETTING:

Healthy volunteer in an academic research environment.

PATIENT(S):

An individual premenopausal woman.

INTERVENTION(S):

Endometrial cultures were grown in collagen gels for 4 weeks, and exposed to various steroid and retinoid treatments.

MAIN OUTCOME MEASURE(S):

Histological features and expression of cytokeratins, vimentin, and reticulin.

RESULT(S):

Cultures developed multiple glands and surface epithelium that exhibited positive cytokeratin and negative vimentin staining. Single stromal cells inside the collagen exhibited negative cytokeratin and positive vimentin staining. Networks of reticulin fibers produced by the cells were increased by estrogen, decreased by progesterone, and unaffected by retinoids. Contraction of the collagen gels was inhibited by retinoids that activated retinoic acid receptors (RARs), but not by a retinoid specific for retinoid X receptors (RXRs). The combination and timing of retinoid and steroid hormone treatments were demonstrated to induce tissue architecture and histological features that resembled either proliferative or secretory phases.

CONCLUSION(S):

Growth of menstrual cells in collagen can be manipulated with retinoids and steroids to resemble histological features of the proliferative and secretory phases.

PMID:
12215339
DOI:
10.1016/s0015-0282(02)03302-2
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center