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Type: Journal article
Title: Lesion development is modulated by the natural estrous cycle and mouse strain in a minimally invasive model of endometriosis
Author: Dodds, K.
Beckett, E.
Evans, S.
Hutchinson, M.
Citation: Biology of Reproduction, 2017; 97(6):810-821
Publisher: Society for the Study of Reproduction
Issue Date: 2017
ISSN: 0006-3363
Statement of
Kelsi N. Dodds, Elizabeth A. H. Beckett, Susan F. Evans and Mark R. Hutchinson
Abstract: Many rodent models of endometriosis are invasive, involving surgery to implant donor endometrial tissue into recipient animals. Moreover, few studies have compared and contrasted lesions between rodent strains and estrous stages without exogenous hormone manipulation. This is despite extensive data demonstrating that genetic and hormonal factors can influence endometriosis progression. Here, we have refined a minimally-invasive model of endometriosis using naturally cycling mice (donor and recipient matched for cycle phase) to investigate lesion development in two different strains (C57BL/6 and Balb/C), induced in estrous stages of high and low estrogen (proestrus or estrus, respectively), and with varying amounts of donor endometrial tissue (7.5-40 mg), injected intraperitoneally. The overall probability of developing endometriosis-like lesions was higher in proestrus than estrus, and increased with greater masses of donor tissue. Similarly, the total number of lesions (0-3) increased from 7.5 to 40 mg, and was significantly greater in proestrus C57BL/6 mice but not Balb/Cs. The dominant lesion type also differed between mouse strains; C57BL/6 mice were more likely to develop dense-type lesions, whereas Balb/C mice developed a greater proportion of cystic-type. This data further supports a role for estrogen in the development of endometriosis, and that genetic variance can influence the degree and characteristics of lesions. Our minimally-invasive model would be beneficial for studies with outcome measurements particularly sensitive to incisional injury, such as pain, or alterations to sex hormones, including fertility.
Keywords: endometriosis; endometrium; mouse model; mouse strain; estrogen; estrous cycle
Description: Advance Access Publication Date: 24 October 2017
Rights: © The Authors 2017. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved
RMID: 0030077043
DOI: 10.1093/biolre/iox132
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Appears in Collections:Physiology publications

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