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Mechanisms of pulmonary fibrosis in PECAM-1 deficient FVB/n mice

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dc.contributor.authorLishnevsky, Marta, author
dc.contributor.authorSchenkel, Alan R., advisor
dc.contributor.authorDow, Steven, committee member
dc.contributor.authorSlayden, Richard, committee member
dc.contributor.authorOrton, Christopher, committee member
dc.date.accessioned2007-01-03T06:38:57Z
dc.date.available2015-06-30T05:57:00Z
dc.date.issued2014
dc.description.abstractIdiopathic Pulmonary Fibrosis (IPF) is a fatal disease of the aging population that affects nearly 100,000 Americans, and its incidence has been steadily on the increase. Patients typically present in late-stage disease, and effective early stage diagnosis and treatment methods are thoroughly lacking. The cellular and molecular events involved in disease initiation are still unknown. There is increasing evidence that alveolar bleeding and coagulation play an important role in the initiation and progression of IPF, and anticoagulant therapies have been shown to exacerbate the process of the disease. Most current mouse models have difficulty in reproducing the spontaneous occurrence of the disease. Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1) deficient mice on the FVB/n background spontaneously develop a fatal chronic pulmonary disease in the absence of a detectable acute inflammatory event. The studies here found that the disease observed in these animals is characterized by alveolar collapse frequently accompanied by extravasated red blood cells in the alveolar space, presence of hemosiderin-positive alveolar macrophages, fibrin deposition, and myofibroblasts in areas of developing collagen deposition. The early events hallmarked by alveolar collapse and extravasated red blood cells in alveoli are of particular importance, as identifying early pathogenic events that lead to the development of fibrotic disease can contribute to the development of preventive, diagnostic, and treatment options for the patient population with IPF.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierLishnevsky_colostate_0053A_12045.pdf
dc.identifier.urihttp://hdl.handle.net/10217/82497
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subjectfibrosis
dc.subjectmicrohemorrhage
dc.subjectmyofibroblasts
dc.subjectoedema
dc.subjecthemosiderin
dc.subjectmacrophages
dc.titleMechanisms of pulmonary fibrosis in PECAM-1 deficient FVB/n mice
dc.typeText
dcterms.embargo.expires2015-06-30
dcterms.embargo.terms2015-06-30
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineMicrobiology, Immunology, and Pathology
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

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