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Effect of 1,25(Oh)2-Vitamin D3 on Expression and Phosphorylation of Progesterone Receptor in Cultured Endometrial Stromal Cells of Patients With Repeated Implantation Failure Publisher Pubmed



Hosseinirad H1 ; Novin MG1 ; Hosseini S2 ; Nazarian H1 ; Amidi F3 ; Paktinat S1 ; Azizi E1 ; Mofarahe ZS1
Authors
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Authors Affiliations
  1. 1. Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  2. 2. Preventative Gynecology Research Center (PGRC), Shahid Beheshti University of Medical Sciences, Tehran, Iran
  3. 3. Department of Anatomical Sciences, School of Medicine, Tehran University of Medical Science, Tehran, Iran

Source: Acta Histochemica Published:2020


Abstract

Repeated implantation failure (RIF) occurs in a condition when good quality embryos fail to implant in the endometrium following several in vitro fertilization (IVF) cycles. Suboptimal endometrial receptivity is one of the main underlying factors that causes this failure. Progesterone is the key regulator of endometrial receptivity which regulates gene expression through binding to its receptors in the endometrial stromal cells (eSC). The aim of this study was to evaluate the effect of 1,25(OH)2-vitamin D3 on progesterone receptor (PR) expression level and its phosphorylation on Ser294 residues in eSC of RIF patients and healthy fertile women. After isolation of the eSC from biopsy samples of RIF patients and healthy fertile women and their characterization, the cells were incubated with vitamin D3 and the expression level of PR mRNA, PR protein and phospho-Ser294 PR protein were evaluated after treatment. The results showed that vitamin D3 treatment increases PR mRNA and protein level and phospho-Ser294 PR protein level in the isolated eSC of both RIF patients and the control group. These results suggest that vitamin D3 may possibly play a key role during the embryo implantation process by affecting the expression pattern and regulatory modifications of the PR in the eSC. © 2019 Elsevier GmbH