Search Results
You are looking at 1 - 2 of 2 items for
- Author: Rocío Martínez-Aguilar x
- Refine by access: All content x
Search for other papers by Rocío Martínez-Aguilar in
Google Scholar
PubMed
Centre for Inflammation Research, University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK
Search for other papers by Lucy E Kershaw in
Google Scholar
PubMed
Search for other papers by Jane J Reavey in
Google Scholar
PubMed
Search for other papers by Hilary O D Critchley in
Google Scholar
PubMed
Search for other papers by Jacqueline A Maybin in
Google Scholar
PubMed
The endometrium is a multicellular tissue that is exquisitely responsive to the ovarian hormones. The local mechanisms of endometrial regulation to ensure optimal function are less well characterised. Transient physiological hypoxia has been proposed as a critical regulator of endometrial function. Herein, we review the literature on hypoxia in the non-pregnant endometrium. We discuss the pros and cons of animal models, human laboratory studies and novel in vivo imaging for the study of endometrial hypoxia. These research tools provide mounting evidence of a transient hypoxic episode in the menstrual endometrium and suggest that endometrial hypoxia may be present at the time of implantation. This local hypoxia may modify the inflammatory environment, influence vascular remodelling and modulate endometrial proliferation to optimise endometrial function. Finally, we review current knowledge of the impact of this hypoxia on endometrial pathologies, with a focus on abnormal uterine bleeding. Throughout the manuscript areas for future research are highlighted with the aim of concentrating research efforts to maximise future benefits for women and society.
Search for other papers by Maria Jose Ruiz Magaña in
Google Scholar
PubMed
Search for other papers by Jose Maria Puerta in
Google Scholar
PubMed
Search for other papers by Rocio Martínez-Aguilar in
Google Scholar
PubMed
Search for other papers by Tatiana Llorca in
Google Scholar
PubMed
Search for other papers by Osmany Blanco in
Google Scholar
PubMed
Search for other papers by Raquel Muñoz-Fernández in
Google Scholar
PubMed
Departamento de Bioquímica y Biología Molecular III e Inmunología, Universidad de Granada, Granada, Spain
Unidad de Gestión Clínica Laboratorios, Hospital Universitario Clínico San Cecilio, Granada, Spain
Search for other papers by Enrique G Olivares in
Google Scholar
PubMed
Departamento de Bioquímica y Biología Molecular III e Inmunología, Universidad de Granada, Granada, Spain
Search for other papers by Carmen Ruiz-Ruiz in
Google Scholar
PubMed
Endometrial stromal cells (EnSCs) and decidual stromal cells (DSCs) originate from fibroblastic precursors located around the vessels of the human nonpregnant endometrium and the pregnant endometrium (decidua), respectively. Under the effect of ovarian or pregnancy hormones, these precursors differentiate (decidualize), changing their morphology and secreting factors that appear to be essential for the normal development of pregnancy. However, the different physiological context – that is, non-pregnancy vs pregnancy – of those precursors (preEnSCs, preDSCs) might affect their phenotype and functions. In the present study, we established preEnSC and preDSC lines and compared the antigen phenotype and responses to decidualization factors in these two types of stromal cell line. Analyses with flow cytometry showed that preEnSCs and preDSCs exhibited a similar antigen phenotype compatible with that of bone marrow mesenchymal stem/stromal cells. The response to decidualization in cultures with progesterone and cAMP was evaluated by analyzing changes in cell morphology by microscopy, prolactin and IL-15 secretion by enzyme immunoassay and the induction of apoptosis by flow cytometry. In all four analyses, preDSCs showed a significantly higher response than preEnSCs. The expression of progesterone receptor (PR), protein kinase A (PKA) and FOXO1 was studied with Western blotting. Both types of cells showed similar levels of PR and PKA, but the increase in PKA RI subunit expression in response to decidualization was again significantly greater in preDSCs. We conclude that preEnSCs and preDSCs are equivalent cells but differ in their ability to decidualize. Functional differences between them probably derive from factors in their different milieus.
