A murine model of acute lung injury identifies growth factors to promote tissue repair and their biomarkers.

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  • Additional Information
    • Source:
      Publisher: Blackwell Science Ltd Country of Publication: England NLM ID: 9607379 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2443 (Electronic) Linking ISSN: 13569597 NLM ISO Abbreviation: Genes Cells Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford, UK : Blackwell Science Ltd., 1996-
    • Subject Terms:
      Bone Marrow Transplantation* ; Metabolome*; Acute Lung Injury/*prevention & control ; Alveolar Epithelial Cells/*cytology ; Biomarkers/*metabolism ; Heparin-binding EGF-like Growth Factor/*physiology ; Intercellular Signaling Peptides and Proteins/*metabolism; Acute Lung Injury/chemically induced ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Animals ; Diphtheria Toxin/toxicity ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muramidase/genetics ; Promoter Regions, Genetic ; Wound Healing
    • Abstract:
      Type II alveolar epithelial cells (AEC2s) play a crucial role in the regeneration of type I AECs after acute lung injury. The mechanisms underlying the regeneration of AEC2s are not fully understood. To address this issue, here, we investigated a murine model of acute lung injury using mice expressing human Diphtheria Toxin Receptor (DTR) under the control of Lysozyme M promoter (LysM-DTR). DT injection induced the depletion of AEC2s, alveolar macrophages, and bone marrow (BM)-derived myeloid cells in LysM-DTR mice, and the mice died within 6 days after DT injection. Apoptotic AEC2s and bronchiolar epithelial cells appeared at 24 hr, whereas Ki67-positive proliferating cells appeared in the alveoli and bronchioles in the lung of LysM-DTR mice at 72-96 hr after DT injection. Transfer of wild-type BM cells into LysM-DTR mice accelerated the regeneration of AEC2s along with the up-regulation of several growth factors. Moreover, several metabolites were significantly decreased in the sera of LysM-DTR mice compared with WT mice after DT injection, suggesting that these metabolites might be biomarkers to predict AEC2s injury. Together, LysM-DTR mice might be useful to identify growth factors to promote lung repair and the metabolites to predict the severity of lung injury.
      (© 2018 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd.)
    • Grant Information:
      17H04069 Grants-in-Aid for Scientific Research (B); 17K19533 Challenging Exploratory Research; Japan Society for the Promotion of Science (JSPS); 26110003 Scientific Research on Innovative Areas; JP18gm1210002 Japan Agency for Medical Research and Development (AMED) through AMED-CREST; Private University Research Branding project; MEXT (Ministry of Education, Culture, Sports, Science and Technology), Japan; Ministry of Health, Labour and Welfare of Japan; Study Group on Diffuse Pulmonary Disorders; Scientific Research/Research on intractable diseases
    • Contributed Indexing:
      Keywords: Diphtheria toxin receptor; apoptosis; biomarker; bronchiolar epithelial cell; growth factors; interleukin 11; lung injury; tissue repair; type II alveolar epithelial cell (AEC)
    • Accession Number:
      0 (Biomarkers)
      0 (Diphtheria Toxin)
      0 (Heparin-binding EGF-like Growth Factor)
      0 (Intercellular Signaling Peptides and Proteins)
      EC 3.2.1.17 (Muramidase)
      EC 3.2.1.17 (lysozyme M, mouse)
    • Publication Date:
      Date Created: 20181127 Date Completed: 20190423 Latest Revision: 20190423
    • Publication Date:
      20240105
    • Accession Number:
      10.1111/gtc.12659
    • Accession Number:
      30474194