- Title:
- MiR-145 suppresses embryo-epithelial juxtacrine communication at implantation by modulating maternal IGF1R
- Journal:
- J Cell Sci. 2015 Feb 15;128(4):804-14
- Author(s):
- Kang YJ1, Lees M2, Matthews LC3, Kimber SJ4, Forbes K5, Aplin JD5
- Author(s) affiliation:
- 1Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, UK St Mary's Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, UK Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Level 3, Women's Centre, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK.
2Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, UK St Mary's Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, UK.
3Centre for Endocrinology & Diabetes, Institute of Human Development, University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, UK.
4Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK.
5Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, Manchester M13 9WL, UK St Mary's Hospital, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester M13 9WL, UK This email address is being protected from spambots. You need JavaScript enabled to view it. This email address is being protected from spambots. You need JavaScript enabled to view it..
Abstract taken from PubMed
- Abstract:
- Successful implantation requires the synchronization of viable embryonic development with endometrial receptivity. The mechanisms allowing for the initiation of crosstalk between the embryo and the endometrium remain elusive, however recent studies have revealed alterations in endometrial microRNAs (miRs) in women suffering repeated implantation failure; one of the altered miRs is miR-145. We assessed the role of miR-145 and its target, IGF1R, in early implantation. miR-145 overexpression and IGF1R knockdown were achieved in Ishikawa endometrial cells. QPCR, western blotting and 3′UTR luciferase reporter assays confirmed that IGF1R is a direct target of miR-145 in the endometrium. Attachment of mouse embryos or IGF-I-coated beads to endometrial epithelial cells was used to study the effects of altered miR-145 and/or IGF1R expression on early implantation events. miR-145 overexpression or specific reduction of IGF1R impaired attachment in both cases. miR-145/IGF1R target protectors prevented miR-145-mediated reduction in IGF1R and reversed the effect of miR-145 overexpression on attachment. The data demonstrate that miR-145 influences embryo attachment by reducing the level of IGF1R in endometrium.
- Link to the paper on PubMed
