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New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis
BACKGROUND: Endometriosis can lead to infertility. Since there is no definitive treatment for endometriosis, animal modelling seems necessary to examine the possible treatments. Mouse endometrium cannot be separated for endometriosis induction. In addition, transplantation of uterus into the abdomin...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8446700/ https://www.ncbi.nlm.nih.gov/pubmed/34557653 http://dx.doi.org/10.1002/ame2.12181 |
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author | Abdolmaleki, Amir Jalili, Cyrus Mansouri, Kamran Bakhtiari, Mitra |
author_facet | Abdolmaleki, Amir Jalili, Cyrus Mansouri, Kamran Bakhtiari, Mitra |
author_sort | Abdolmaleki, Amir |
collection | PubMed |
description | BACKGROUND: Endometriosis can lead to infertility. Since there is no definitive treatment for endometriosis, animal modelling seems necessary to examine the possible treatments. Mouse endometrium cannot be separated for endometriosis induction. In addition, transplantation of uterus into the abdominal viscera to induce endometriosis causes organ damage. In this study, we defined a new model of endometriosis leading to separability of endometrium and a safe anatomical region for transplantation. METHODS: Forty female mice were allocated to 5 groups: 1, sham; 2, allograft uterus transplantation of mice to anterior abdominal wall of mice; 3, allograft uterus transplantation of mice to mesentery of mice; 4, xenograft endometrial transplantation of rat to anterior abdominal wall of mice; 5, xenograft endometrial transplantation of rat to mesentery of mice. Adult female rats with a previous pregnancy experience were selected and placed in the vicinity of male rats for 2 weeks to induce estrogen secretion and increase endometrial thickness. RESULTS: In the 4th group of animals, compared to sham, the peritoneal concentrations of VEGF‐A, TNF‐α, NO, MDA, and serum levels of CA‐125 and IL‐37 were increased and total body weight was decreased, while weight and size of endometrial lesions were increased significantly (P < .05). Genes expression of HOXA10 and HOXA11 were decreased significantly (P < .05) in groups 2 and 4 compared to sham. CONCLUSIONS: Xenograft transplantation of endometrium from rat to anterior abdominal wall of mice can potentially mimic human endometriosis morphologically, histologically, and genetically. |
format | Online Article Text |
id | pubmed-8446700 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84467002021-09-22 New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis Abdolmaleki, Amir Jalili, Cyrus Mansouri, Kamran Bakhtiari, Mitra Animal Model Exp Med Original Articles BACKGROUND: Endometriosis can lead to infertility. Since there is no definitive treatment for endometriosis, animal modelling seems necessary to examine the possible treatments. Mouse endometrium cannot be separated for endometriosis induction. In addition, transplantation of uterus into the abdominal viscera to induce endometriosis causes organ damage. In this study, we defined a new model of endometriosis leading to separability of endometrium and a safe anatomical region for transplantation. METHODS: Forty female mice were allocated to 5 groups: 1, sham; 2, allograft uterus transplantation of mice to anterior abdominal wall of mice; 3, allograft uterus transplantation of mice to mesentery of mice; 4, xenograft endometrial transplantation of rat to anterior abdominal wall of mice; 5, xenograft endometrial transplantation of rat to mesentery of mice. Adult female rats with a previous pregnancy experience were selected and placed in the vicinity of male rats for 2 weeks to induce estrogen secretion and increase endometrial thickness. RESULTS: In the 4th group of animals, compared to sham, the peritoneal concentrations of VEGF‐A, TNF‐α, NO, MDA, and serum levels of CA‐125 and IL‐37 were increased and total body weight was decreased, while weight and size of endometrial lesions were increased significantly (P < .05). Genes expression of HOXA10 and HOXA11 were decreased significantly (P < .05) in groups 2 and 4 compared to sham. CONCLUSIONS: Xenograft transplantation of endometrium from rat to anterior abdominal wall of mice can potentially mimic human endometriosis morphologically, histologically, and genetically. John Wiley and Sons Inc. 2021-09-03 /pmc/articles/PMC8446700/ /pubmed/34557653 http://dx.doi.org/10.1002/ame2.12181 Text en © 2021 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Abdolmaleki, Amir Jalili, Cyrus Mansouri, Kamran Bakhtiari, Mitra New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title | New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title_full | New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title_fullStr | New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title_full_unstemmed | New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title_short | New rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
title_sort | new rat to mouse xenograft transplantation of endometrium as a model of human endometriosis |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8446700/ https://www.ncbi.nlm.nih.gov/pubmed/34557653 http://dx.doi.org/10.1002/ame2.12181 |
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