Lishnevsky, Marta, authorSchenkel, Alan R., advisorDow, Steven, committee memberSlayden, Richard, committee memberOrton, Christopher, committee member2007-01-032015-06-302014http://hdl.handle.net/10217/82497Idiopathic 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.born digitaldoctoral dissertationsengCopyright 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.fibrosismicrohemorrhagemyofibroblastsoedemahemosiderinmacrophagesText