Literature DB >> 11163839

Use of knockout transgenic mice in the study of endometriosis: insights from mice lacking beta(2)-microglobulin and interleukin-12p40.

E Somigliana1, P Viganò, P Filardo, M Candiani, M Vignali, P Panina-Bordignon.   

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.

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Year:  2001        PMID: 11163839     DOI: 10.1016/s0015-0282(00)01659-9

Source DB:  PubMed          Journal:  Fertil Steril        ISSN: 0015-0282            Impact factor:   7.329


  10 in total

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Journal:  Am J Pathol       Date:  2011-09-13       Impact factor: 4.307

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3.  Transcriptional regulation of Na+/H+ exchanger expression in the intact mouse.

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4.  Macrophages are alternatively activated in patients with endometriosis and required for growth and vascularization of lesions in a mouse model of disease.

Authors:  Monica Bacci; Annalisa Capobianco; Antonella Monno; Lucia Cottone; Francesca Di Puppo; Barbara Camisa; Margherita Mariani; Chiara Brignole; Mirco Ponzoni; Stefano Ferrari; Paola Panina-Bordignon; Angelo A Manfredi; Patrizia Rovere-Querini
Journal:  Am J Pathol       Date:  2009-07-02       Impact factor: 4.307

5.  Endometriosis, a disease of the macrophage.

Authors:  Annalisa Capobianco; Patrizia Rovere-Querini
Journal:  Front Immunol       Date:  2013-01-28       Impact factor: 7.561

6.  Platelets induce increased estrogen production through NF-κB and TGF-β1 signaling pathways in endometriotic stromal cells.

Authors:  Qiuming Qi; Xishi Liu; Qi Zhang; Sun-Wei Guo
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7.  Changing prostaglandin E2 (PGE2) signaling during lesional progression and exacerbation of endometriosis by inhibition of PGE2 receptor EP2 and EP4.

Authors:  Qingqing Huang; Xishi Liu; Sun-Wei Guo
Journal:  Reprod Med Biol       Date:  2021-12-02

8.  Gut microbiota-derived short-chain fatty acids protect against the progression of endometriosis.

Authors:  Sangappa B Chadchan; Pooja Popli; Chandrasekhar R Ambati; Eric Tycksen; Sang Jun Han; Serdar E Bulun; Nagireddy Putluri; Scott W Biest; Ramakrishna Kommagani
Journal:  Life Sci Alliance       Date:  2021-09-30

9.  Tetramethylpyrazine Retards the Progression and Fibrogenesis of Endometriosis.

Authors:  Shenghui Huang; Fengyi Xiao; Sun-Wei Guo; Tingting Zhang
Journal:  Reprod Sci       Date:  2022-01-31       Impact factor: 3.060

10.  Early maternal separation accelerates the progression of endometriosis in adult mice.

Authors:  Qiqi Long; Xishi Liu; Sun-Wei Guo
Journal:  Reprod Biol Endocrinol       Date:  2020-06-12       Impact factor: 5.211

  10 in total

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