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Biomedicines
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Animal Models of Endometriosis, from the Bench to the Clinic
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Animal Models of Endometriosis, from the Bench to the Clinic

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 12226

Special Issue Editor

Dr. Rául Goḿez

E-Mail Website
Guest Editor
Research Unit on Women’s Health-Institute of Health Research, INCLIVA, 46010 Valencia, Spain
Interests: endometrial cancer, endometriosis, animal models, immunotherapy, RANK, angiogenesis, fertility, pain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Animal models are a key platform for exploring pathways involved in the onset and progression of endometriosis, as well as for the development and testing of drugs with clinical therapeutic potential. Studies exploring pathways in the progression of endometriosis, testing the effects of drugs on pain or lesion size, setting up and refining new animal models, and similar approaches contributing to advances in endometriosis knowledge fall under the scope of this Special Issue—with the unique condition that animal models are employed as the basis for the research performed.

Dr. Rául Goḿez
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  •  endometriosis
  •  animal models
  •  pain
  •  lesion size
  •  immunology
  •  angiogenesis
  •  extracellular matrix
  •  physiology
  •  ROS
  •  inflammation
  •  natural medicine
  •  therapeutics

Published Papers (6 papers)

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Research

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10 pages, 1931 KiB  
Article
Impact of Chronic Exposure to Endometriosis on Perinatal Outcomes: Establishment of a Mouse Model
by Mohammed Elsherbini, Kaori Koga, Eiko Maki, Keiichi Kumasawa, Erina Satake, Ayumi Taguchi, Tomoko Makabe, Arisa Takeuchi, Gentaro Izumi, Masashi Takamura, Miyuki Harada, Tetsuya Hirata, Yasushi Hirota, Osamu Wada-Hiraike and Yutaka Osuga
Biomedicines 2022, 10(10), 2627; https://doi.org/10.3390/biomedicines10102627 - 19 Oct 2022
Cited by 4 | Viewed by 1617
Abstract
The purpose of this study was to establish a new mouse model of endometriosis that mimics real-world women’s health problems, in which women continue to be affected by endometriosis long before they wish to become pregnant, and to evaluate the impact of “chronic [...] Read more.
The purpose of this study was to establish a new mouse model of endometriosis that mimics real-world women’s health problems, in which women continue to be affected by endometriosis long before they wish to become pregnant, and to evaluate the impact of “chronic exposure to endometriosis” on perinatal outcome. Endometriosis was established by the intraperitoneal injection of homologous minced mouse uteri. Vehicle was injected for the control. Mating was initiated either 1 or 43 days after disease establishment (Young or Aged studies, respectively). Mice were sacrificed on 18 dpc. The number pups and resorptions were counted and pups’ body weights (BW) were measured, and the endometriosis lesion was identified and weighted. In the Young study, the number of resorptions and BW were comparable between the groups. In the Aged study, the number of resorptions was significantly higher and BW was significantly lower in endometriosis than that in control. The total weight of endometriosis lesion per dam was significantly lower in the Aged compared to the Young endometriosis group; however, not a single mouse was found to have any lesions at all. These results suggest that in addition to the presence of endometriosis per se, “chronic exposure to endometriosis” prior to pregnancy affect perinatal outcomes. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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13 pages, 2571 KiB  
Article
Leptin Stimulates Endometriosis Development in Mouse Models
by Tae Hoon Kim, Nayoung Bae, Taeho Kim, Albert L. Hsu, Mark I. Hunter, Jung-Ho Shin and Jae-Wook Jeong
Biomedicines 2022, 10(9), 2160; https://doi.org/10.3390/biomedicines10092160 - 01 Sep 2022
Cited by 4 | Viewed by 2013
Abstract
Endometriosis is a chronic inflammatory condition in women, and obesity leads to an inflammatory condition that is directly involved in the etiology of endometriosis. However, observational studies have shown an inverse correlation between endometriosis and a low body mass index (BMI). Obesity does [...] Read more.
Endometriosis is a chronic inflammatory condition in women, and obesity leads to an inflammatory condition that is directly involved in the etiology of endometriosis. However, observational studies have shown an inverse correlation between endometriosis and a low body mass index (BMI). Obesity does not protect against endometriosis, and on the contrary, an increased BMI may lead to more severe forms of the disease. To determine the effect of obesity on endometriosis, diet-induced and genetically engineered obese mouse models were integrated with endometriosis mouse models with fluorescence-tagged ectopic lesions. High-fat diet-induced obese mice revealed a significant increase in endometriosis development compared with regular-diet control mice. However, obese recipient mice with leptin deficiency and leptin receptor deficiency showed suppressed endometriosis development compared with control mice. Furthermore, donor uterine tissues with leptin deficiency and leptin receptor deficiency suppressed endometriosis development compared with control donor in control recipient mice. Importantly, we revealed that aberrant high levels of leptin concentration significantly increased endometriosis development compared with vehicle treatment group in control mice with normal body weight. Our results suggest that leptin and its receptor are critical for endometriosis development. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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21 pages, 5819 KiB  
Article
Perioperative Suppression of Schwann Cell Dedifferentiation Reduces the Risk of Adenomyosis Resulting from Endometrial–Myometrial Interface Disruption in Mice
by Xi Wang, Xishi Liu and Sun-Wei Guo
Biomedicines 2022, 10(6), 1218; https://doi.org/10.3390/biomedicines10061218 - 24 May 2022
Cited by 5 | Viewed by 1945
Abstract
We have recently demonstrated that endometrial–myometrial interface (EMI) disruption (EMID) can cause adenomyosis in mice, providing experimental evidence for the well-documented epidemiological finding that iatrogenic uterine procedures increase the risk of adenomyosis. To further elucidate its underlying mechanisms, we designed this study to [...] Read more.
We have recently demonstrated that endometrial–myometrial interface (EMI) disruption (EMID) can cause adenomyosis in mice, providing experimental evidence for the well-documented epidemiological finding that iatrogenic uterine procedures increase the risk of adenomyosis. To further elucidate its underlying mechanisms, we designed this study to test the hypothesis that Schwann cells (SCs) dedifferentiating after EMID facilitate the genesis of adenomyosis, but the suppression of SC dedifferentiation perioperatively reduces the risk. We treated mice perioperatively with either mitogen-activated protein kinase kinase (MEK)/extracellular-signal regulated protein kinase (ERK) or c-Jun N-terminal kinase (JNK) inhibitors or a vehicle 4 h before and 24 h, 48 h and 72 h after the EMID procedure. We found that EMID resulted in progressive SCs dedifferentiation, concomitant with an increased abundance of epithelial cells in the myometrium and a subsequent epithelial–mesenchymal transition (EMT). This EMID-induced change was abrogated significantly with perioperative administration of JNK or MEK/ERK inhibitors. Consistently, perioperative administration of a JNK or a MEK/ERK inhibitor reduced the incidence by nearly 33.5% and 14.3%, respectively, in conjunction with reduced myometrial infiltration of adenomyosis and alleviation of adenomyosis-associated hyperalgesia. Both treatments significantly decelerated the establishment of adenomyosis and progression of EMT, fibroblast-to-myofibroblast trans-differentiation and fibrogenesis in adenomyotic lesions. Thus, we provide the first piece of evidence strongly implicating the involvement of SCs in the pathogenesis of adenomyosis induced by EMID. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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Review

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16 pages, 868 KiB  
Review
The Unmet Needs for Studying Chronic Pelvic/Visceral Pain Using Animal Models
by Ana Catarina Neto, Mariana Santos-Pereira, Pedro Abreu-Mendes, Delminda Neves, Henrique Almeida, Francisco Cruz and Ana Charrua
Biomedicines 2023, 11(3), 696; https://doi.org/10.3390/biomedicines11030696 - 24 Feb 2023
Cited by 2 | Viewed by 1551
Abstract
The different definitions of chronic pelvic/visceral pain used by international societies have changed over the years. These differences have a great impact on the way researchers study chronic pelvic/visceral pain. Recently, the role of systemic changes, including the role of the central nervous [...] Read more.
The different definitions of chronic pelvic/visceral pain used by international societies have changed over the years. These differences have a great impact on the way researchers study chronic pelvic/visceral pain. Recently, the role of systemic changes, including the role of the central nervous system, in the perpetuation and chronification of pelvic/visceral pain has gained weight. Consequently, researchers are using animal models that resemble those systemic changes rather than using models that are organ- or tissue-specific. In this review, we discuss the advantages and disadvantages of using bladder-centric and systemic models, enumerating some of the central nervous system changes and pain-related behaviors occurring in each model. We also present some drawbacks when using animal models and pain-related behavior tests and raise questions about possible, yet to be demonstrated, investigator-related bias. We also suggest new approaches to study chronic pelvic/visceral pain by refining existing animal models or using new ones. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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15 pages, 342 KiB  
Review
What We Have Learned from Animal Models to Understand the Etiology and Pathology of Endometrioma-Related Infertility
by Zhouyurong Tan, Sze-Wan Hung, Xu Zheng, Chi-Chiu Wang, Jacqueline Pui-Wah Chung and Tao Zhang
Biomedicines 2022, 10(7), 1483; https://doi.org/10.3390/biomedicines10071483 - 23 Jun 2022
Cited by 1 | Viewed by 2550
Abstract
Endometrioma (OMA) is the most common subtype of endometriosis, in which the endometriotic lesions are implanted in the ovary. Women with OMA are usually associated with infertility, presenting with reduced ovarian reserve, low oocyte quantity and quality, and poor fertility outcomes. However, the [...] Read more.
Endometrioma (OMA) is the most common subtype of endometriosis, in which the endometriotic lesions are implanted in the ovary. Women with OMA are usually associated with infertility, presenting with reduced ovarian reserve, low oocyte quantity and quality, and poor fertility outcomes. However, the underlying pathological mechanisms in OMA-related infertility are still unclear. Due to the limitations and ethical issues of human studies in reproduction, animal models that recapitulate OMA characteristics and its related infertility are critical for mechanistic studies and subsequent drug development, preclinical testing, and clinical trials. This review summarized the investigations of OMA-related infertility based on previous and latest endometrioma models, providing the possible pathogenesis and potential therapeutic targets for further studies. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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Graphical abstract

Other

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9 pages, 1053 KiB  
Brief Report
Dissecting the miR-451a-Mif Pathway in Endometriosis Pathophysiology Using a Syngeneic Mouse Model: Temporal Expression of Lesion Mif Receptors, Cd74 and Cxcr4
by Warren B. Nothnick and Amanda Graham
Biomedicines 2022, 10(7), 1699; https://doi.org/10.3390/biomedicines10071699 - 14 Jul 2022
Cited by 2 | Viewed by 1507
Abstract
Endometriosis is an enigmatic disease characterized by pain and infertility in which endometrial tissue grows in ectopic locations, predominantly the pelvic cavity. The pathogenesis and pathophysiology of endometriosis is complex and postulated to involve alterations in inflammatory, cell proliferation and post-transcriptional regulatory pathways [...] Read more.
Endometriosis is an enigmatic disease characterized by pain and infertility in which endometrial tissue grows in ectopic locations, predominantly the pelvic cavity. The pathogenesis and pathophysiology of endometriosis is complex and postulated to involve alterations in inflammatory, cell proliferation and post-transcriptional regulatory pathways among others. Our understanding on the pathogenesis and pathophysiology of endometriosis is further complicated by the fact that endometriosis can only be diagnosed by laparoscopy only after the disease has manifested. This makes it difficult to understand the true pathogenesis as a cause-and-effect relationship is difficult to ascertain. To aid in our understanding on endometriosis pathogenesis and pathophysiology, numerous rodent models have been developed. In this case, we discuss further assessment of a miR-451a—macrophage migration inhibitory factor (Mif) pathway which contributes to lesion survival. Specifically, we evaluate the temporal expression of lesion Mif receptors, Cd74 and Cxcr4 using host mice which express wild-type or miR-451a deficient lesions. Similar to that observed in humans and a non-human primate model of endometriosis, Cd74 expression is elevated in lesion tissue in a temporal fashion while that of Cxcr4 shows minimal increase during initial lesion establishment but is reduced later during the lifespan. Absence of miR-451a during initial lesion establishment is associated with an augmentation of Cd74, but no Cxcr4 expression. The data obtained in this study provide further support for a role of Mif receptors, Cd74 and Cxcr4 in the pathophysiology of endometriosis. Full article
(This article belongs to the Special Issue Animal Models of Endometriosis, from the Bench to the Clinic)
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