OBJECTIVE: To compare the expression of endometrial P receptors (PR) levels with markers of endometrial receptivity during the window of implantation. DESIGN: Prospective, controlled study to examine endometrial PR and three cycle-specific integrins in endometrial biopsies obtained during the window of implantation. SETTING: An academic teaching hospital. PATIENTS: One hundred seventy-five endometrial biopsies from regularly cycling women with luteal phase defect (LPD; group 1; n = 80), medically treated LPD (group 2; n = 16), minimal and mild endometriosis with aberrant alpha v beta 3 expression (group 3; n = 21), fertile controls (group 4; n = 26), and infertile controls (group 5; n = 32). MAIN OUTCOME MEASURE: Immunohistochemical staining intensity of each antigen using the semi-quantitative grading system (HSCORE), compared using analysis of variance with Scheffe's correction. RESULTS: Among the five groups studied, nuclear PR expression was significantly elevated in glandular epithelial cells from tissue samples with histologic delay > or = 3 days consistent with luteal phase deficiency (LPD; group 1). Failure of PR down-regulation was associated with aberrant alpha v beta 3 integrin expression. Medical correction of LPD was associated with return of normal endometrial histology, normal integrin expression, and the loss of epithelial PR, similar to controls. The other two cycle-dependent integrin markers, alpha 1 beta 1 and alpha 4 beta 1, were not different between groups. In women with aberrant alpha v beta 3 and "in phase" endometrium, epithelial PR expression was not different from controls. CONCLUSIONS: The establishment of normal endometrial receptivity appears to be tightly associated with the down-regulation of epithelial PR. Histologic delay, consistent with LPD, is associated with a failure of PR down-regulation and the lack of normal markers of endometrial receptivity. Occult uterine receptivity defects (aberrant beta 3 expression in otherwise normal histology) are regulated differently, suggesting alternate mechanisms also exist which influence endometrial receptivity.
OBJECTIVE: To compare the expression of endometrial P receptors (PR) levels with markers of endometrial receptivity during the window of implantation. DESIGN: Prospective, controlled study to examine endometrial PR and three cycle-specific integrins in endometrial biopsies obtained during the window of implantation. SETTING: An academic teaching hospital. PATIENTS: One hundred seventy-five endometrial biopsies from regularly cycling women with luteal phase defect (LPD; group 1; n = 80), medically treated LPD (group 2; n = 16), minimal and mild endometriosis with aberrant alpha v beta 3 expression (group 3; n = 21), fertile controls (group 4; n = 26), and infertile controls (group 5; n = 32). MAIN OUTCOME MEASURE: Immunohistochemical staining intensity of each antigen using the semi-quantitative grading system (HSCORE), compared using analysis of variance with Scheffe's correction. RESULTS: Among the five groups studied, nuclear PR expression was significantly elevated in glandular epithelial cells from tissue samples with histologic delay > or = 3 days consistent with luteal phase deficiency (LPD; group 1). Failure of PR down-regulation was associated with aberrant alpha v beta 3 integrin expression. Medical correction of LPD was associated with return of normal endometrial histology, normal integrin expression, and the loss of epithelial PR, similar to controls. The other two cycle-dependent integrin markers, alpha 1 beta 1 and alpha 4 beta 1, were not different between groups. In women with aberrant alpha v beta 3 and "in phase" endometrium, epithelial PR expression was not different from controls. CONCLUSIONS: The establishment of normal endometrial receptivity appears to be tightly associated with the down-regulation of epithelial PR. Histologic delay, consistent with LPD, is associated with a failure of PR down-regulation and the lack of normal markers of endometrial receptivity. Occult uterine receptivity defects (aberrant beta 3 expression in otherwise normal histology) are regulated differently, suggesting alternate mechanisms also exist which influence endometrial receptivity.
Authors: Paul B Miller; Brent A Parnell; Greta Bushnell; Nicholas Tallman; David A Forstein; H Lee Higdon; Jo Kitawaki; Bruce A Lessey Journal: Hum Reprod Date: 2012-01-13 Impact factor: 6.918
Authors: Koji Yoshinaga; Mercy PrabhuDas; Christopher Davies; Kenneth White; Kathleen Caron; Thaddeus Golos; Asgerally Fazleabas; Bibhash Paria; Gil Mor; Soumen Paul; Xiaoqin Ye; Sudhansu K Dey; Thomas Spencer; Robert Michael Roberts Journal: Am J Reprod Immunol Date: 2013-11-29 Impact factor: 3.886
Authors: Jason W Ross; Morgan D Ashworth; Daniel Mathew; Patrick Reagan; Jerry W Ritchey; Kanako Hayashi; Thomas E Spencer; Matthew Lucy; Rodney D Geisert Journal: Reprod Biol Endocrinol Date: 2010-04-28 Impact factor: 5.211