Abstract
Objectives
The cyclical changes in proliferation and differentiation of endometrial cells are
regulated by estrogen and progesterone via modulating Wnt/β-catenin signaling. Imbalance
in the expression of estrogen and progesterone receptors causes progesterone resistance
in endometriosis patients. The aim of this study was to investigate the expression
of some main components of Wnt/β-catenin signaling including WNT7a, DKK-1, β-catenin,
and GSK-3β in eutopic endometrium and peritoneal endometriotic lesions of endometriosis
patients compared to healthy endometrium in the mid-secretory phase of menstrual cycle.
Study Design
This prospective study was performed, during a 12 months period from December 2015
to November 2016, on healthy women as the control group (n = 14) and endometriosis patients (n = 34). We used real-time polymerase chain reaction and Western blot techniques.
Results
Protein and mRNA expression of DKK-1 were significantly down-regulated in both endometriotic
lesions and eutopic endometrium of endometriosis group. We also demonstrated that
the expression of non-phosphorylated β-catenin (active form) and phosphorylated GSK-3β
(inactive form) were up-regulated in endometriosis patients. The mRNA levels of β-catenin,
GSK-3β, and WNT7a, as well as the protein levels of total β-catenin, total GSK-3β,
and WNT7a in endometriosis group, were not significantly different with those in control
group. The patterns of mRNA and protein expression of all interested factors in the
lesions were similar to those in the eutopic endometrium of same patients.
Conclusions
It seems that the aberrant activation of Wnt/β-catenin signaling in the secretory
phase of the menstrual cycle in endometriosis has two essential elements: excessive
inactivation of GSK-3β and suppression of the expression of Wnt signaling inhibitor
DKK-1. Interventions in this signaling pathway may allow for the exploration of potential
new targets for the control of development and progression of endometriosis.
Keywords
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Article info
Publication history
Published online: October 31, 2017
Accepted:
October 30,
2017
Received in revised form:
October 5,
2017
Received:
May 29,
2017
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.