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Am J Physiol Lung Cell Mol Physiol 284: L926-L937, 2003. First published January 24, 2003; doi:10.1152/ajplung.00247.2002
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Vol. 284, Issue 6, L926-L937, June 2003

Role of VEGF-B in the lung during development of chronic hypoxic pulmonary hypertension

Vanessa Louzier1, Bernadette Raffestin2, Aude Leroux3, Didier Branellec3, Jean Michel Caillaud3, Micheline Levame1, Saadia Eddahibi1, and Serge Adnot1

1 Département de Physiologie, Institut National de la Santé et de La Recherche Médicale Unité 492, Hôpital Henri Mondor, Assistance Publique-Hôpitaux de Paris, 94010 Créteil; 2 Département de Physiologie, Unité de Formation et de Recherche Paris-Ile de France Ouest, Hôpital Ambroise Paré, Assistance Publique-Hôpitaux de Paris, 92104 Boulogne; and 3 Département de Thérapie Génique Cardio-Vasculaire, Gencell, France

Angiogenic factors exert protective effects on the lung. To investigate the effect of VEGF-B, a factor coexpressed in the lung with VEGF-A, we assessed chronic hypoxic pulmonary hypertension in VEGF-B knockout mice (VEGF-B-/-) and in rats with lung overexpression of VEGF-B induced by adenovirus transfer. No significant difference in pulmonary hemodynamics, right ventricular hypertrophy, distal vessel muscularization, or vascular density was found between VEGF-B-/- and control mice after 3 wk of hypoxia. When overexpressed, VEGF-B167 or VEGF-B186 had protective effects similar to those of human VEGF-A165. Lung endothelial nitric oxide synthase (eNOS) expression was increased by 5 days of hypoxia or VEGF-A adenovirus vector (Ad.VEGF-A) overexpression, whereas VEGF-B167 or VEGF-B186 had no effect. With hypoxia or normoxia, the wet-to-dry lung weight ratio was increased 5 days after Ad.VEGF-A administration compared with control (Ad.nul), Ad.VEGF-B167, or Ad.VEGF-B186. Endogenous VEGF-B does not counteract the development of hypoxic pulmonary hypertension. However, when overexpressed in the lung, VEGF-B can be as potent as VEGF-A in attenuating pulmonary hypertension, although it has no effect on eNOS expression or vascular permeability.

adenoviral transfer; angiogenic factors


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