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1 Developmental Lung Biology, University of Colorado health Sciences Center, Denver, Colorado, USA
2 Developmental Lung Biology, University of Colorado health Sciences Center, Denver, Colorado, USA; Division of Pulmonary Sciences, University of Colorado Health Center, Denver, Colorado, USA
3 California National Primate Research Center, University of California, Davis, California, USA
4 Hematologic Malignancies, John Hopkins Oncology Center, Baltimore, Maryalnd, USA
* To whom correspondence should be addressed. E-mail: neil.davie{at}uchsc.edu.
Information is rapidly emerging regarding the important role of the arterial vasa vasorum in a variety of systemic vascular diseases. In addition, increasing evidence suggests that progenitor cells of bone marrow (BM) origin may contribute to post-natal neovascularization and/or vascular wall thickening that is characteristic in some forms of systemic vascular disease. Little is known regarding post-natal vasa formation and the role of BM-derived progenitor cells in the setting of pulmonary hypertension (PH). We sought to determine the effects of chronic hypoxia on the density of vasa vasorum in the pulmonary artery and to evaluate if BM-derived progenitor cells contribute to the increased vessel wall mass in a bovine model of hypoxia-induced PH. Quantitative morphometric analyses of lung tissue from normoxic and hypoxic calves revealed that hypoxia results in a dramatic expansion of the pulmonary artery adventitial vasa vasorum. Flow cytometric analysis demonstrated that cells expressing the transmembrane tyrosine kinase receptor for stem cell factor, c-kit, are mobilized from the BM into the circulation in response to hypoxia. Immunohistochemistry revealed an increase in the expression of c-kit+ cells together with vascular endothelial growth factor, fibronectin and thrombin in the hypoxia-induced remodeled pulmonary artery vessel wall. Circulating mononuclear cells isolated from neonatal calves exposed to hypoxia were found to differentiate into endothelial and smooth muscle cell phenotypes depending on culture conditions. From these observations, we suggest that the vasa vasorum and circulating progenitor cells could be involved in vessel wall thickening in the setting of hypoxia-induced PH.
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