Steroid receptor and aromatase expression in baboon endometriotic lesions.
OBJECTIVE
To evaluate steroid receptor and aromatase gene expression in endometriotic lesions, and determine the effects of endometriosis on uterine receptivity in a baboon model for endometriosis.


METHODS
Prospective study to determine the expression of steroid receptors, and aromatase in ectopic endometriotic lesions and endometrial genes in the eutopic endometrium of baboons with induced endometriosis by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry.


METHODS
University research laboratory and primate research facility.


METHODS
Normally cycling baboons inoculated intraperitoneally with menstrual endometrium to induce endometriosis.


METHODS
Endometriotic lesions were resected during laparotomy, and endometrium was obtained by endometrectomy or after hysterectomy.


METHODS
Steroid receptor and aromatase expression by RT-PCR and immunocytochemistry in endometriotic lesions and glycodelin and alpha-smooth muscle actin expression and localization in endometrium after chorionic gonadotropin (CG) stimulation.


RESULTS
This study demonstrated that estrogen receptor-alpha (ERalpha) and progesterone receptor (PR) were expressed in both ectopic and eutopic endometrium between 1 and 10 months after inoculation. In contrast, ERbeta was only expressed in the ectopic endometriotic lesions. Aromatase expression was only evident in lesions obtained 10 months after inoculation. Infusion of CG during the luteal phase failed to induce the expression of glycodelin in the glandular epithelium or alpha-smooth muscle actin (alpha-SMA) in stromal cells in animals with endometriosis as early as 1 and 4 months after inoculation.


CONCLUSIONS
The ERbeta expression is selectively up-regulated in the endometriotic lesions at all stages of the disease, whereas aromatase expression is not evident until the disease progresses. However, expression of uterine receptivity markers was down-regulated as early as 1 and 4 months after inoculation.
D000199:Actins / Q000378:metabolism; D000818:Animals; D001141:Aromatase / Q000096:biosynthesis* / Q000235:genetics; D015139:Blotting, Southern; D004715:Endometriosis / Q000201:enzymology / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D005260:Female; D006023:Glycoproteins / Q000378:metabolism; D007150:Immunohistochemistry; D010215:Papio / Q000378:metabolism*; D011257:Pregnancy Proteins / Q000378:metabolism; D011446:Prospective Studies; D012313:RNA / Q000737:chemistry / Q000235:genetics; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000235:genetics; D011980:Receptors, Progesterone / Q000096:biosynthesis / Q000235:genetics; D011987:Receptors, Steroid / Q000096:biosynthesis* / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
D000199:Actins; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D006023:Glycoproteins; D011257:Pregnancy Proteins; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011987:Receptors, Steroid; C101118:progesterone receptor A; C097314:progesterone receptor B; D012313:RNA; D001141:Aromatase