First evidence of a menstruating rodent: the spiny mouse (Acomys cahirinus)

Bellofiore, Nadia; Ellery, Stacey J.; Mamrot, Jared; Walker, David W.; Temple-Smith, Peter; Dickinson, Hayley

doi:10.1530/repabs.3.p064

Cited by 18 publications

(35 citation statements)

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“…Female rodents do not undergo a menstrual cycle with shedding of the endometrium akin to humans (with the exception of the spiny mouse [5]). Rather, an estrous cycle where the endometrium, in the absence of implantation, is reabsorbed by the activity of infiltrating leukocytes.…”

Section: Introductionmentioning

confidence: 99%

Lesion development is modulated by the natural estrous cycle and mouse strain in a minimally invasive model of endometriosis†

Dodds

Beckett

Evans

et al. 2017

Biology of Reproduction

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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. These data further support 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.

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Section: Introductionmentioning

confidence: 99%

Lesion development is modulated by the natural estrous cycle and mouse strain in a minimally invasive model of endometriosis†

Dodds

Beckett

Evans

et al. 2017

Biology of Reproduction

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“…Among the rodents, only one species has been described as menstruating: the spiny mouse, Acomys cahirinus. 41 This is surprising, given the large number of rodent species (2277 species). Then there is a small number of bat species belonging to 2 groups of bats, 1 molossid bats and 3 phyllostomid bats.…”

Section: The Evolutionary History Of Menstruationmentioning

confidence: 99%

“…However, in humans, decidualization occurs even in the absence of an embryo and is therefore called spontaneous decidualization. It turns out that all menstruating species undergo spontaneous decidualization, 40,41,52 suggesting that the evolved trait is not menstruation per se, but spontaneous decidualization. In humans, it has been shown that the proximate cause for menstruation (see section on Menstruation and abnormal uterine bleeding) is the decrease in progesterone levels owing to the degeneration of the corpus luteum.…”

Section: Why Did Menstruation Evolve?mentioning

confidence: 99%

Menstruation: science and society

Critchley

Babayev

Bulun

et al. 2020

American Journal of Obstetrics and Gynecology

176

119

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H.O.D.C. has clinical research support for laboratory consumables and staff from Bayer AG and provides consultancy advice (but with no personal remuneration) for Bayer AG, PregLem SA, Gedeon Richter, Vifor Pharma UK Ltd, AbbVie Inc, and Myovant Sciences GmbH. H.O.D.C. receives royalties from UpToDate for article on abnormal uterine bleeding. A.K. receives royalties from UpToDate, Wolters Kluwer for work on the topic hysterosalpingography. E.E.M. consults for Myovant Sciences. K.A.M. is coinvestigator for Bayer Essure longitudinal research study and clinical trial (all funds for this research go to the site of research [W.I.H.] e no personal compensation). K.A.M. is scientific advisor for Myovant (advises on patient questionnaires related to AUB-compensation goes to employer [C.N.E.M.G.]-no personal compensation). K.A.M. has received honoraria from ABOG, ACOG, and NIH for participating in working groups and meetings. K.A.M. is HHS Office of Population Affairs Title X Grant Reviewer (received honorarium). I.M. is employee of Igenomix R&D. C.S. is Head of the Igenomix Scientific Advisory Board. The other authors report no conflict of interest.

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“…Differential regulation of the initiation and maintenance genes suggest differences in control of placental development between mouse and human. The Spiny mouse does menstruate, which may make it an attractive model for future research on early implantation events (Bellofiore et al, ). However, the many similarities between mouse and human placenta make mTSC an alternative choice to model the effect of stress on early placentation.…”

Section: Comparison Of Mouse and Human Placentamentioning

confidence: 99%

Hypoxic Stress Forces Adaptive and Maladaptive Placental Stress Responses in Early Pregnancy

Abdulhasan

Awonuga

et al. 2017

Birth Defects Research

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This review focuses on hypoxic stress and its effects on the placental lineage and the earliest differentiation events in mouse and human placental trophoblast stem cells (TSCs). Although the placenta is a decidual organ at the end of pregnancy, its earliest rapid growth and function at the start of pregnancy precedes and supports growth and function of the embryo. Earliest function requires that TSCs differentiate, however, "hypoxia" supports rapid growth, but not differentiation of TSCs. Most of the literature on earliest placental "hypoxia" studies used 2% oxygen which is normoxic for TSCs. Hypoxic stress happens when oxygen level drops below 2%. It decreases anabolism, proliferation, potency/stemness and increases differentiation, despite culture conditions that would sustain proliferation and potency. Thus, to study the pathogenesis due to TSC dysfunction, it is important to study hypoxic stress below 2%. Many studies have been performed using 0.5 to 1% oxygen in cultured mouse TSCs. From all these studies, a small number has examined human trophoblast lines and primary first trimester placental hypoxic stress responses in culture. Some other stress stimuli, aside from hypoxic stress, are used to elucidate common and unique aspects of hypoxic stress. The key outcomes produced by hypoxic stress are mitochondrial, anabolic, and proliferation arrest, and this is coupled with stemness loss and differentiation. Hypoxic stress can lead to depletion of stem cells and miscarriage, or can lead to later dysfunctions in placentation and fetal development. Birth Defects Research 109:1330-1344, 2017. © 2017 Wiley Periodicals, Inc.

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First evidence of a menstruating rodent: the spiny mouse (Acomys cahirinus)

Cited by 18 publications

References 0 publications

Lesion development is modulated by the natural estrous cycle and mouse strain in a minimally invasive model of endometriosis†

Lesion development is modulated by the natural estrous cycle and mouse strain in a minimally invasive model of endometriosis†

Menstruation: science and society

Hypoxic Stress Forces Adaptive and Maladaptive Placental Stress Responses in Early Pregnancy

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