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1 Departement de physiologie, Institut National de la Sante et de la Recherche Medicale U492, CRETEIL, France
2 Departement de physiologie, Ile de France Ouest, Hopital Ambroise Pare, AP-HP, BOULOGNE, France
3 Departement de therapie genique cardio-vasculaire, Gencell SA, France
* To whom correspondence should be addressed. E-mail: serge.ednot{at}hmn.ap-hop-paris.fr.
Angiogenic factors exert protective effects on the lung. To investigate the effect of VEGF-B, a factor co-expressed in the lung with VEGF-A, we assessed chronic hypoxic pulmonary hypertension in VEGF-B knockout mice 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 weeks of hypoxia. When overexpressed, VEGF-B167 or VEGF-B 186 had protective effects similar to those of human VEGF-A165. Lung eNOS expression was increased by 5 days of hypoxia or Ad.VEGF-A overexpression, whereas VEGF-B167 or VEGF-B 186 had no effect. With hypoxia or normoxia, the wet-to-dry lung weight ratio was increased 5 days after Ad.VEGF-A administration as compared with Ad.nul, Ad.VEGF-B167, or Ad.VEGF-B 186. 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.
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