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Published on: May 23, 2014
Stanniocalcin-1 expression in normal human endometrium and dysregulation in endometriosis
Lusine Aghajanova1, Signe Altmäe2, Sergo Kasvandik3
1Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Francisco, San Francisco, California.
Objective:
To determine expression of stanniocalcin-1 (STC1) in human endometrium with and without endometriosis and its regulation by steroid hormones.
Design:
Laboratory study.
Setting:
University.
Patient(S):
Nineteen women with endometriosis and 33 control women.
Intervention(S):
Endometrial biopsy and fluid sampling.
Main Outcome Measure(S):
Analysis of early secretory (ESE) and midsecretory (MSE) endometrial secretomes from fertile women with the use of nano-liquid chromatography-dual mass spectrometry; real-time quantitative polymerase chain reaction, and immunohistochemistry for STC1 and its receptor calcium-sensing receptor (CASR) mRNA and proteins in endometrium with and without endometriosis; evaluation of STC1 and CASR mRNA expression in endometrial stromal fibroblasts (eSF) from women with and without endometriosis decidualized with the use of E2P or 8-bromo-cyclic adenosine monophosphate (cAMP).
Result(S):
STC1 protein was strongly up-regulated in MSE versus ESE in endometrial fluid of fertile women. STC1 mRNA significantly increased in MSE from women with, but not from those without, endometriosis, compared with proliferative endometrium or ESE, with no significant difference throughout the menstrual cycle between groups. STC1 mRNA in eSF from control women increased >230-fold on decidualization with the use of cAMP versus 45-fold from women with endometriosis, which was not seen on decidualization with E2/P. CASR mRNA did not exhibit significant differences in any condition and was not expressed in isolated eSF. STC1 protein immunoexpression in eSF was significantly lower in women with endometriosis compared with control women.
Conclusion(S):
STC1 protein is significantly up-regulated in MSE endometrial fluid and is dysregulated in eutopic endometrial tissue from women with endometriosis. It is likely regulated by cAMP and may be involved in the pathogenesis of decidualization defects.
