Redistribution of corticotropin-releasing hormone receptor R2 using fluorescence immunohistochemistry in fetal membranes of women delivering preterm or at term.

OBJECTIVE

The aim of our study was to determine whether a difference exists in expression of corticotropin-releasing hormone receptor-R1 (CRH-R1) and corticotropin-releasing hormone receptor-R2 (CRH-R2) in fetal membranes of preterm and term women with or without labor.

MATERIAL AND METHODS

Small pleces of fetal membranes were obtained from the placenta of each of forty patients undergoing cesarean section. Ten samples each were taken from preterm and term patients, with and without labor. Antibodies against CRH-R1/2 and CRH-R2 were used for localization by conventional fluorescence immunohistochemistry. The evaluation of staining was based on examination of the entire histologic section by three independent observers.

RESULTS

In women at term without labor, CRH-R2 receptor was predominantly expressed in the amniotic epithelium and the amniotic mesenchyme. In laboring women at term, the expression of CRH-R2 receptor was shown in the chorionic mesenchyme and the cytotrophoblast cells, but no specific staining could be detected in the amniotic membranes. Changes in CRH-R2 receptor expression could not be demonstrated during preterm labor of early pregnancies. In preterm women, the antibody against CRH-R1/2 receptor detected additional signals in the amniotic mesenchyme and epithelium, suggesting expression of CRH-R1 in these tissues. In women at term, the overlapping pattern of CRH-R1/2 was recognized in both the chorionic and amniotic mesenchyme, in contrast to the specific CRH-R2 staining, suggesting expression of CRH-R1 in the mesodermal cell compartments.

CONCLUSION

At term, changes in CRH-R2 expression are directly related to the progression of normal labor; such changes were not observed during preterm labor of early pregnancies. The increased CRH-R2 expression in the chorionic mesenchyme may possibly provoke rupture of the membranes or at least play a role in some key regulatory events in the initiation of normal labor. The fact that this mechanism does not occur in preterm labor strengthens the hypothesis that onset of labor could be controlled by distinct mechanisms in preterm and term pregnancies.