Proliferation of Endometrial Stromal Cells in Adenomyosis
2 other identifiers
observational
45
1 country
1
Brief Summary
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.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P25-P50 for all trials
Started Sep 2005
Shorter than P25 for all trials
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
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Study Timeline
Key milestones and dates
Study Start
First participant enrolled
September 1, 2005
CompletedFirst Submitted
Initial submission to the registry
September 12, 2005
CompletedFirst Posted
Study publicly available on registry
September 15, 2005
CompletedStudy Completion
Last participant's last visit for all outcomes
March 1, 2006
CompletedSeptember 15, 2005
May 1, 2005
September 12, 2005
September 12, 2005
Conditions
Keywords
Eligibility Criteria
You may qualify if:
- women with adenomyosis
- at early- to mid-secretory phases
You may not qualify if:
- postmenopausal
- malignancy
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (1)
National Taiwan University Hospital
Taipei, Taiwan
MeSH Terms
Conditions
Condition Hierarchy (Ancestors)
Study Officials
- PRINCIPAL INVESTIGATOR
Jehn-Hsiahn Yang, M.D.
Department of Obstetrics and Gynecology, National Taiwan University Hospital
Study Design
- Study Type
- observational
- Observational Model
- DEFINED POPULATION
- Time Perspective
- OTHER
- Sponsor Type
- OTHER
Study Record Dates
First Submitted
September 12, 2005
First Posted
September 15, 2005
Study Start
September 1, 2005
Study Completion
March 1, 2006
Last Updated
September 15, 2005
Record last verified: 2005-05