- ICH GCP
- US Clinical Trials Registry
- Clinical Trial NCT00173212
Proliferation of Endometrial Stromal Cells in Adenomyosis
Adenomyosis refers to the presence of endometrial glands and stroma that is haphazardly deep within the myometrium. However, the etiology and pathologic mechanism responsible for adenomyosis are not yet very well known. Our previous results revealed that the expression of killer inhibitory receptors on natural killer cells was decreased in eutopic endometrium in women with adenomyosis. It implies that the formation of adenomyosis might be due to abnormal endometrial tissues, but not the aberrant local immunological dysfunction in myometrium. Our further investigation revealed that in vitro coculture of macrophages and endometrial stromal cells (ESCs) increase the expression of IL-6 mRNA in ESC, which might further enhance the proliferation of ESC and subsequently result in the formation of ectopic endometrial implants in adenomyosis.
Abnormal cell proliferation has been generally found in the tumorigenesis, including the formation of endometriosis. Adenomyosis is considered to have a similar pathophysiology with endometriosis, and it must be interesting to examine whether there is abnormal cell proliferation in the eutopic endometrium of adenomyosis. Lipopolysaccharide (LPS) was found to promote proliferation of ESCs via induction of TNF-a and IL-8 expression, whereas IFN-g significantly inhibited ESCs proliferation. Therefore, whether abnormal cell proliferation occurs under the effects of LPS and IFN-g in the eutopic endometrium of adenomyosis needs further clarification.
Adenomyosis preferentially affects women between the ages of 35 and 50 years, and the symptoms subside gradually after menopause. It is well known that there is a close conjunction between estrogen and adenomyosis. Estradiol (E2) was demonstrated to induce endometrial cell proliferation, whereas medroxyprogesterone (MPA) inhibited endometrial cell proliferation via antagonizing estrogenic effects. Experiments to investigate these steroid effects on ESC proliferation in vitro in the eutopic endometrium of adenomyosis are of clinical relevance.
In this study, we try to collect endometrial tissues from women with and without adenomyosis, and then purify ESCs from endometrium. ESCs are cultured for 2 days with the supplement of LPS, IFN-gamma, Estradiol, MPA and Estradiol+MPA. Quantification of cell proliferation was done with Cell Proliferation Assay Kit and immunocytochemical detection of Ki-67, in an attempt to examine the cell proliferation of ESCs in women with adenomyosis.
Study Overview
Status
Conditions
Detailed Description
Eutopic endometrium was obtained and separated into single endometrial stromal cell (ESC) in women with adenomyosis (study group) and without adenomyosis (control group).
ESCs are cultured for 2 days with the supplement of LPS, IFN-gamma, Estradiol, MPA and Estradiol+MPA.
Quantification of cell proliferation was done with Cell Proliferation Assay Kit and immunocytochemical detection of Ki-67.
Study Type
Enrollment
Contacts and Locations
Study Locations
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Taipei, Taiwan
- National Taiwan University Hospital
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Participation Criteria
Eligibility Criteria
Ages Eligible for Study
Accepts Healthy Volunteers
Genders Eligible for Study
Description
Inclusion Criteria:
- women with adenomyosis
- at early- to mid-secretory phases
Exclusion Criteria:
- postmenopausal
- malignancy
Study Plan
How is the study designed?
Design Details
Collaborators and Investigators
Study record dates
Study Major Dates
Study Start
Study Completion
Study Registration Dates
First Submitted
First Submitted That Met QC Criteria
First Posted (Estimate)
Study Record Updates
Last Update Posted (Estimate)
Last Update Submitted That Met QC Criteria
Last Verified
More Information
Terms related to this study
Additional Relevant MeSH Terms
Other Study ID Numbers
- 9461700522
- NTUH.95-000357
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