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Transgenic Mice in Human Diseases: Insights from Molecular Research 5.0

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: closed (31 May 2024) | Viewed by 633

Special Issue Editor


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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
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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 (1 paper)

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Research

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 302
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
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