Viewing Study NCT00173212



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Last Modification Date: 2024-10-26 @ 9:16 AM
Study NCT ID: NCT00173212
Status: UNKNOWN
Last Update Posted: 2005-09-15
First Post: 2005-09-12

Brief Title: Proliferation of Endometrial Stromal Cells in Adenomyosis
Sponsor: National Taiwan University Hospital
Organization: National Taiwan University Hospital

Study Overview

Official Title: None
Status: UNKNOWN
Status Verified Date: 2005-05
Last Known Status: ACTIVE_NOT_RECRUITING
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
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 EstradiolMPA 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
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 EstradiolMPA

Quantification of cell proliferation was done with Cell Proliferation Assay Kit and immunocytochemical detection of Ki-67

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None
Secondary IDs
Secondary ID Type Domain Link
NTUH95-000357 None None None