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Transgenic Mice in Human Diseases: Insights from Molecular Research (5th Edition)

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 5016

Special Issue Editor

Dr. Timofey S. Rozhdestvensky

E-Mail Website
Guest Editor
Medical Faculty, Core Facility Transgenic Animal and Genetic Engineering Models (TRAM), University of Muenster, Von-Esmarch-Str. 56, D-48149 Muenster, Germany
Interests: genome editing; CRISPR-Cas9 technology; programmable DNA endonucleases; nervous system diseases; RNA biology; disease-associated RNAs; non-protein coding RNAs; etc.
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Transgenic mouse models are essential for understanding the molecular mechanisms and pathogenicity of most human diseases. Research based on live mouse models is important in terms of discovering and/or improving methods for the prevention, diagnosis, and treatment of diseases.

This Special Issue aims to cover all areas of molecular-based research in order to study various human diseases using genetically engineered mouse models. It welcomes original research, reviews, and short communication articles on cellular and molecular analyses of transgenic mouse models. Areas of interest include, but are not limited to, functional genomics of disease, epigenomics, proteomics, RNA biology, systems biology, approaches to and methods of mouse genome editing, software tools, etc.

Topics of interest for the Issue include:

  • Generation of transgenic mouse models and targeting constructs;
  • Mouse genome editing approaches;
  • Transgenic mouse models in cancer research;
  • Transgenic mouse models to study infectious diseases;
  • Transgenic mouse models for mitochondrial diseases;
  • Transgenic mouse models in:
    • Cardiovascular diseases;
    • Developmental disorders;
    • Digestive system diseases;
    • Endocrine system diseases;
    • Immune diseases;
    • Integumentary system diseases;
    • Lymphatic system diseases;
    • Metabolism, obesity, and metabolic diseases;
    • Nervous system diseases (including sensory organ disorders);
    • Reproductive system diseases;
    • Respiratory system diseases;
    • Skeletal and muscular system diseases;
    • Urinary system diseases.

Dr. Timofey S. Rozhdestvensky
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • transgenic mouse models
  • mouse genome editing
  • transgenic mice
  • mouse models
  • genome editing
  • CRISPR-Cas9 technology

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Published Papers (4 papers)

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Research

17 pages, 5772 KiB  
Article
Knockout of the Carbohydrate Responsive Element Binding Protein Enhances Proliferation and Tumorigenesis in Renal Tubules of Mice
by Kerrin Hansen, Kristin Peters, Christian K. Burkert, Eric Brose, Diego F. Calvisi, Katrina Ehricke, Maren Engeler, Elisa Knuth, Nils Kröger, Andrea Lohr, Jessica Prey, Jenny Sonke, Padmanabhan Vakeel, Juliane Wladasch, Jenny Zimmer, Frank Dombrowski and Silvia Ribback
Int. J. Mol. Sci. 2024, 25(21), 11438; https://doi.org/10.3390/ijms252111438 - 24 Oct 2024
Viewed by 533
Abstract
Glycogen-storing so-called clear cell kidney tubules (CCTs), precursor lesions of renal cell carcinoma, have been described in diabetic rats and in humans. The lesions show upregulation of the Akt/mTOR-pathway and the related transcription factor carbohydrate responsive element binding protein (ChREBP), which is supposedly [...] Read more.
Glycogen-storing so-called clear cell kidney tubules (CCTs), precursor lesions of renal cell carcinoma, have been described in diabetic rats and in humans. The lesions show upregulation of the Akt/mTOR-pathway and the related transcription factor carbohydrate responsive element binding protein (ChREBP), which is supposedly pro-oncogenic. We investigated the effect of ChREBP-knockout on nephrocarcinogenesis in streptozotocin-induced diabetic and normoglycemic mice. Diabetic, but not non-diabetic mice, showed CCTs at 3, 6 and 12 months of age. Glycogenosis was confirmed by periodic acid schiff reaction and transmission electron microscopy. CCTs in ChREBP-knockout mice consisted of larger cells and occurred more frequently compared to wildtype mice. Progression towards kidney tumors was observed in both diabetic groups but occurred earlier in ChREBP-knockout mice. Proliferative activity assessed by BrdU-labeling was lower in 1-week-old but higher in 12-month-old diabetic ChREBP-knockout mice. Surprisingly, renal neoplasms occurred spontaneously in non-diabetic ChREBP-knockout, but not non-diabetic wildtype mice, indicating an unexpected tumor-suppressive function of ChREBP. Immunohistochemistry showed upregulated glycolysis and lipogenesis, along with activated Akt/mTOR-signaling in tumors of ChREBP-knockout groups. Immunohistochemistry of human clear cell renal cell carcinomas revealed reduced ChREBP expression compared to normal kidney tissue. However, the molecular mechanisms by which loss of ChREBP might facilitate tumorigenesis require further investigation. Full article
(This article belongs to the Special Issue Transgenic Mice in Human Diseases: Insights from Molecular Research (5th Edition))
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18 pages, 5004 KiB  
Article
Advancing 3Rs: The Mouse Estrus Detector (MED) as a Low-Stress, Painless, and Efficient Tool for Estrus Determination in Mice
by Irina V. Belozertseva, Dmitrijs D. Merkulovs, Helena Kaiser, Timofey S. Rozhdestvensky and Boris V. Skryabin
Int. J. Mol. Sci. 2024, 25(17), 9429; https://doi.org/10.3390/ijms25179429 - 30 Aug 2024
Viewed by 1349
Abstract
Determining the estrous cycle stages in mice is essential for optimizing breeding strategies, synchronizing experimental timelines, and facilitating studies in behavior, drug testing, and genetics. It is critical for reducing the production of genetically unmodified offspring in the generation and investigation of genetically [...] Read more.
Determining the estrous cycle stages in mice is essential for optimizing breeding strategies, synchronizing experimental timelines, and facilitating studies in behavior, drug testing, and genetics. It is critical for reducing the production of genetically unmodified offspring in the generation and investigation of genetically modified animal models. An accurate detection of the estrus cycle is particularly relevant in the context of the 3Rs—Replacement, Reduction, and Refinement. The estrous cycle, encompassing the reproductive phases of mice, is key to refining experimental designs and addressing ethical issues related to the use of animals in research. This study presents results from two independent laboratories on the efficacy of the Mouse Estrus Detector (MED) from ELMI Ltd. (Latvia) for the accurate determination of the estrus phase. The female mice of five strains/stocks (CD1, FVB/N, C57Bl6/J, B6D2F1, and Swiss) were used. The results showed that the MEDProTM is a low-traumatic, simple, rapid, and painless method of estrus detection that supports the principles of the 3Rs. The use of the MEDProTM for estrus detection in mice caused minimal stress, enhanced mating efficiency, facilitated an increase in the number of embryos for in vitro fertilization, and allowed the production of the desired number of foster animals. Full article
(This article belongs to the Special Issue Transgenic Mice in Human Diseases: Insights from Molecular Research (5th Edition))
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18 pages, 3794 KiB  
Article
Implications of Genetic Factors Underlying Mouse Hydronephrosis: Cautionary Considerations on Phenotypic Interpretation in Genetically Engineered Mice
by Shino Nemoto, Kazuyo Uchida and Hiroshi Ohno
Int. J. Mol. Sci. 2024, 25(13), 7203; https://doi.org/10.3390/ijms25137203 - 29 Jun 2024
Viewed by 944
Abstract
Hydronephrosis, the dilation of kidneys due to abnormal urine retention, occurs spontaneously in certain inbred mouse strains. In humans, its occurrence is often attributed to acquired urinary tract obstructions in adults, whereas in children, it can be congenital. However, the genetic factors underlying [...] Read more.
Hydronephrosis, the dilation of kidneys due to abnormal urine retention, occurs spontaneously in certain inbred mouse strains. In humans, its occurrence is often attributed to acquired urinary tract obstructions in adults, whereas in children, it can be congenital. However, the genetic factors underlying hydronephrosis pathogenesis remain unclear. We investigated the cause of hydronephrosis by analyzing tetraspanin 7 (Tspan7) gene-modified mice, which had shown a high incidence of hydronephrosis-like symptoms. We found that these mice were characterized by low liver weights relative to kidney weights and elevated blood ammonia levels, suggesting liver involvement in hydronephrosis. Gene expression analysis of the liver suggested that dysfunction of ornithine transcarbamylase (OTC), encoded by the X chromosome gene Otc and involved in the urea cycle, may contribute as a congenital factor in hydronephrosis. This OTC dysfunction may be caused by genomic mutations in X chromosome genes contiguous to Otc, such as Tspan7, or via the genomic manipulations used to generate transgenic mice, including the introduction of Cre recombinase DNA cassettes and cleavage of loxP by Cre recombinase. Therefore, caution should be exercised in interpreting the hydronephrosis phenotype observed in transgenic mice as solely a physiological function of the target gene. Full article
(This article belongs to the Special Issue Transgenic Mice in Human Diseases: Insights from Molecular Research (5th Edition))
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12 pages, 4675 KiB  
Article
TGF-β Signalling Regulates Cytokine Production in Inflammatory Cardiac Macrophages during Experimental Autoimmune Myocarditis
by Karolina Tkacz, Filip Rolski, Monika Stefańska, Kazimierz Węglarczyk, Rafał Szatanek, Maciej Siedlar, Gabriela Kania and Przemysław Błyszczuk
Int. J. Mol. Sci. 2024, 25(11), 5579; https://doi.org/10.3390/ijms25115579 - 21 May 2024
Viewed by 1344
Abstract
Myocarditis is characterized by an influx of inflammatory cells, predominantly of myeloid lineage. The progression of myocarditis to a dilated cardiomyopathy is markedly influenced by TGF-β signalling. Here, we investigate the role of TGF-β signalling in inflammatory cardiac macrophages in the development of [...] Read more.
Myocarditis is characterized by an influx of inflammatory cells, predominantly of myeloid lineage. The progression of myocarditis to a dilated cardiomyopathy is markedly influenced by TGF-β signalling. Here, we investigate the role of TGF-β signalling in inflammatory cardiac macrophages in the development of myocarditis and post-inflammatory fibrosis. Experimental autoimmune myocarditis (EAM) was induced in the LysM-Cre × R26-stop-EYFP × Tgfbr2-fl/fl transgenic mice showing impaired TGF-β signalling in the myeloid lineage and the LysM-Cre × R26-stop-EYFP control mice. In EAM, immunization led to acute myocarditis on day 21, followed by cardiac fibrosis on day 40. Both strains showed a similar severity of myocarditis and the extent of cardiac fibrosis. On day 21 of EAM, an increase in cardiac inflammatory macrophages was observed in both strains. These cells were sorted and analysed for differential gene expression using whole-genome transcriptomics. The analysis revealed activation and regulation of the inflammatory response, particularly the production of both pro-inflammatory and anti-inflammatory cytokines and cytokine receptors as TGF-β-dependent processes. The analysis of selected cytokines produced by bone marrow-derived macrophages confirmed their suppressed secretion. In conclusion, our findings highlight the regulatory role of TGF-β signalling in cytokine production within inflammatory cardiac macrophages during myocarditis. Full article
(This article belongs to the Special Issue Transgenic Mice in Human Diseases: Insights from Molecular Research (5th Edition))
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