Use of knockout transgenic mice in the study of endometriosis: insights from mice lacking beta(2)-microglobulin and interleukin-12p40
Lab / animal
OA: closed
CC0
⤵ 17 in-corpus citations
AI-generated summary
This study utilized knockout mice lacking β2-microglobulin and interleukin-12p40 to investigate their roles in the development and progression of endometriosis.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
OBJECTIVE: To test the possibility of using transgenic knockout mice in the study of endometriosis and to investigate specific immunologic aspects of the disease.
DESIGN: Experimental blinded study.
SETTING: Academic research center.
ANIMAL(S): Thirty-two mice with experimentally induced endometriosis.
INTERVENTION(S): Endometriosis was induced in 8 beta(2)-microglobulin-deficient BALB/c mice and 7 wild-type BALB/c controls. Similarly, endometriosis was induced in 8 interleukin-12-deficient C57BL/6 mice and in 9 wild-type C57BL/6 controls.
MAIN OUTCOME MEASURE(S): Weight and surface area of endometriotic lesions.
RESULT(S): Total weight and surface area of endometriotic lesions was markedly lower in beta(2)-microglobulin-deficient BALB/c mice than in wild-type BALB/c controls. A slight but statistically insignificant increase in total weight and surface area of lesions was observed in interleukin-12-deficient C57BL/6 mice compared to wild-type C57BL/6 controls.
CONCLUSION(S): Knockout transgenic mice can be used successfully for the study of endometriosis; however, in these animals, the redundancy of the immunologic cytokine-mediated regulatory mechanisms may lead to compensation from the remaining genome. Results from beta(2)-microglobulin-deficient mice support the critical role of the immune system in the pathogenesis of the disease.
My notes (saved in your browser only)
Condition tags
MeSH descriptors
Citation neighborhood (2-hop)
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]
References (5)
- Endometrial ability to implant in ectopic sites can be prevented by interleukin-12 in a murine model of endometriosis via openalex
- Interleukin-12 and its free p40 subunit regulate immune recognition of endometrial cells: potential role in endometriosis via openalex
- W1990653743 via openalex
- W2010724066 via openalex
- W2020086511 via openalex
Cited by (17)
- A role for gut mycobiome and altered fungal-bacterial interactions in women with endometriosis† 2025
- Identification of distinct stool metabolites in women with endometriosis for non-invasive diagnosis and potential for microbiota-based therapies 2024
- Changing prostaglandin E2 (PGE2) signaling during lesional progression and exacerbation of endometriosis by inhibition of PGE2 receptor EP2 and EP4 2021
- Preoperative and perioperative intervention reduces the risk of recurrence of endometriosis in mice caused by either incomplete excision or spillage and dissemination 2021
- Early maternal separation accelerates the progression of endometriosis in adult mice 2020
- Platelets induce increased estrogen production through NF-κB and TGF-β1 signaling pathways in endometriotic stromal cells 2020
- Sodium tanshinone IIA sulfonate restrains fibrogenesis through induction of senescence in mice with induced deep endometriosis 2020
- Perioperative Intervention by β-Blockade and NF-κB Suppression Reduces the Recurrence Risk of Endometriosis in Mice Due to Incomplete Excision 2019
- Crocin improves endometriosis by inhibiting cell proliferation and the release of inflammatory factors 2018
- Chronic stress accelerates the development of endometriosis in mouse through adrenergic receptor β2 2016
- Progressive development of endometriosis and its hindrance by anti-platelet treatment in mice with induced endometriosis 2016
- Platelets are an unindicted culprit in the development of endometriosis: clinical and experimental evidence 2015
- Endometriosis, a disease of the macrophage 2013
- Proangiogenic Tie2(+) macrophages infiltrate human and murine endometriotic lesions and dictate their growth in a mouse model of the disease 2011
- Macrophages are alternatively activated in patients with endometriosis and required for growth and vascularization of lesions in a mouse model of disease 2009
- Quantification of endometriotic lesions in a murine model by fluorimetric and morphometric analyses 2005
- Distinct mechanisms regulate cyclooxygenase-1 and -2 in peritoneal macrophages of women with and without endometriosis 2002
Source provenance
- europepmc
- last seen: 2026-10-21T06:16:17.486033+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-10-08T20:59:46.244316+00:00
- unpaywall
- last seen: 2026-09-17T06:32:46.214484+00:00
License: CC0
· commercial use OK