Aquaporin 1 is expressed in the human endometrium during normal cycle and increases after mifepristone treatment.

Aquaporin-1 (AQP1) is involved in the angiogenesis and structural modifications of microvessels and possibly also in the pathogenesis of idiopathic menhorrhagia, where a reduced AQP1 expression is seen in the endometrium. Mifepristone treatment induces reduced menstrual bleeding and amenorrhea and also has a direct effect on endometrial arterioles. Administered with gestagen-only contraceptive methods, antiprogestins improve the bleeding pattern. The objective of this study was to evaluate the AQP1 expression in endometrial blood vessels during normal cycle and after mifepristone treatment. Localization and expression of AQP1 was determined using immunohistochemistry and reverse transcriptase chain reaction (RT-PCR) in 43 biopsies from human endometrium taken during a normal cycle and after mifepristone treatment. AQP1 expression in human endometrial vessels is not cycle dependent and is stronger in capillaries and arteries than in veins. After mifepristone treatment the staining intensity was increased, but not the number of stained vessels. The presence of AQP1 was also confirmed using RT-PCR. The changes in AQP1 expression could contribute to the reduced bleeding seen following mifepristone treatment and could be an effect of either antagonizing progesterone or cortisol.

Expression of aquaporin-1 in endometrial blood vessels in menorrhagia.

Aquaporin-1 (AQP1) is a water channel protein expressed in vascular endothelia and involved in impaired angiogenesis in tumors. Since angiogenesis is an essential component of the regeneration of the endometrium, we sought to analyze the expression of AQP1 in endometrial blood vessels in normal cyclic endometrium as well as in endometrial biopsies of menorrhagia patients. Endometrial biopsies from 16 patients with menorrhagia and 21 healthy fertile women were used for immunohistochemistry assessment of AQP1-stained endothelial structures. RT-PCR was used to confirm the presence of AQP1 mRNA. We detected the expression of AQP1 solely in endometrial blood vessels in the control group, as well as in menorrhagic endometrium. There was no difference between proliferative and secretory endometrium. Furthermore, we observed that the vascular expression of AQP1 in endometrial blood vessels in the menorrhagia group was significantly lower than in controls (p=0.002). There was also a significantly lower number of stained vessels per unit area in the menorrhagia group than in the controls (p=0.006). Thus, the deregulation of aquaporin-1 in menorrhagia may be involved in abnormal endometrial vascular growth and permeability.

Expression of aquaporin 2 in human endometrium.

OBJECTIVE: To study the expression of aquaporin-2 (AQP2) in human endometrium. DESIGN: Prospective clinical study. SETTING: Hospital-based unit for gynecology and obstetrics and research laboratories. PATIENT(S): Healthy women with proven fertility who were divided into four groups according to LH peak. INTERVENTION(S): Endometrial biopsies were obtained from 34 women on cycle days LH+4 to LH+14. MAIN OUTCOME MEASURE(S): Localization of AQP2 in human endometrium during normal cycle using immunohistochemistry, verification of AQP2 expression through detection of AQP2 mRNA in reverse transcriptase-polymerase chain reaction (RT-PCR), detection of pinopodes using scanning electron microscopy, and confirmation of AQP2 on pinopodes in confocal microscopy. RESULT(S): Immunostaining of AQP2 is present in the luminal and glandular epithelium but not in the stroma. Some vessels stained positive for AQP2. When present, pinopodes stained positive, which was confirmed using confocal microscopy. A significant increase in staining intensity was seen in the glandular and luminal epithelium during the mid and late luteal phases of the cycle. The presence of AQP2 in human endometrium was also confirmed by RT-PCR. CONCLUSION(S): AQP2 is present in the human endometrium. The expression of AQP2 appears to be cycle dependent and suggests a role for AQP2 in implantation, edema, and/or menstruation.