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Crnkovic, S; Hrzenjak, A; Marsh, LM; Olschewski, A; Kwapiszewska, G.
Origin of neomuscularized vessels in mice exposed to chronic hypoxia.
Respir Physiol Neurobiol. 2011; 179(2-3):342-345 Doi: 10.1016/j.resp.2011.09.016
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Führende Autor*innen der Med Uni Graz
Crnkovic Slaven
Kwapiszewska-Marsh Grazyna
Co-Autor*innen der Med Uni Graz
Hrzenjak Andelko
Marsh Leigh
Olschewski Andrea
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Abstract:
Exposure of mice to chronic hypoxia is one of the most often used animal models to study pulmonary hypertension. Hypoxia exposure leads to vascular remodeling and muscularization of the small parenchymal vessels in the lung. Due to the anatomical differences between mice and humans, it is not possible to determine whether the remodeled vessels originate from the arterial or venous side of the vasculature. By applying antibodies against specific marker molecules expressed by arterial (ephrinB2) and venous (EphB4) endothelial cells, we could show that remodeled parenchymal vessels in hypoxia-exposed mice are mostly of arterial origin with slight venous involvement. Using these tools, it is possible to further characterize remodeled vessels in other small animal models, such as transgenic or knockout mice. Particularly useful applications would include selection of parenchymal vessels for laser microdissection studies. Copyright © 2011 Elsevier B.V. All rights reserved.
Find related publications in this database (using NLM MeSH Indexing)
Airway Remodeling - physiology
Animals -
Arteries - metabolism
Biomarkers - analysis
Chronic Disease -
Disease Models, Animal -
Ephrins - analysis
Ephrins - metabolism
Hypertension, Pulmonary - etiology
Hypertension, Pulmonary - metabolism
Hypertension, Pulmonary - pathology
Hypoxia - complications
Hypoxia - pathology
Immunohistochemistry -
Lung - blood supply
Lung - pathology
Male -
Mice -
Neovascularization, Pathologic - etiology
Neovascularization, Pathologic - pathology
Veins - metabolism

Find related publications in this database (Keywords)
Chronic hypoxia
Pulmonary vascular remodeling
EphrinB2
EphB4
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