The Role of Pericytes in Lipopolysaccharide-Induced Murine Acute Respiratory Distress Syndrome.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0370502 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1525-2191 (Electronic) Linking ISSN: 00029440 NLM ISO Abbreviation: Am J Pathol Subsets: MEDLINE
    • Publication Information:
      Publication: 2011-: New York : Elsevier
      Original Publication: Philadelphia [etc.] American Assn. of Pathologists [etc.]
    • Subject Terms:
      Pericytes*/pathology ; Pericytes*/metabolism ; Respiratory Distress Syndrome*/pathology ; Respiratory Distress Syndrome*/chemically induced ; Respiratory Distress Syndrome*/metabolism ; Lipopolysaccharides*/pharmacology; Animals ; Mice ; Lung/pathology ; Lung/metabolism ; Mice, Inbred C57BL ; Male ; Disease Models, Animal ; Signal Transduction ; Endothelial Cells/metabolism ; Endothelial Cells/pathology
    • Abstract:
      Acute respiratory distress syndrome (ARDS) is a heterogeneous clinical syndrome that is most commonly triggered by infection-related inflammation. Lung pericytes can respond to infection and act as immune and proangiogenic cells; moreover, these cells can differentiate into myofibroblasts in nonresolving ARDS and contribute to the development of pulmonary fibrosis. Here, we aimed to characterize the role of lung cells, which present characteristics of pericytes, such as peri-endothelial location and expression of a panel of specific markers. A murine model of lipopolysaccharide (LPS)-induced resolving ARDS was used to study their role in ARDS. The development of ARDS was confirmed after LPS instillation, which was resolved 14 days after onset. Immunofluorescence and flow cytometry showed early expansion of neural-glial antigen 2 + β-type platelet-derived growth factor receptor + pericytes in murine lungs with loss of CD31 + β-type platelet-derived growth factor receptor + endothelial cells. These changes were accompanied by specific changes in lung structure and loss of vascular integrity. On day 14 after ARDS onset, the composition of pericytes and endothelial cells returned to baseline values. LPS-induced ARDS activated NOTCH signaling in lung pericytes, the inhibition of which during LPS stimulation reduced the expression of its downstream target genes, pericyte markers, and angiogenic factors. Together, these data indicate that lung pericytes in response to inflammatory injury activate NOTCH signaling that supports their maintenance and in turn can contribute to recovery of the microvascular endothelium.
      Competing Interests: Disclosure Statement None declared.
      (Copyright © 2024 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)
    • Accession Number:
      0 (Lipopolysaccharides)
    • Publication Date:
      Date Created: 20240505 Date Completed: 20240727 Latest Revision: 20240813
    • Publication Date:
      20240814
    • Accession Number:
      10.1016/j.ajpath.2024.04.004
    • Accession Number:
      38705380