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(The FASEB Journal. 2001;15:427-438.)
© 2001 FASEB

Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death-dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension

LAIMUTE TARASEVICIENE-STEWART*, YASUNORI KASAHARA{dagger}, LORI ALGER*, PETER HIRTH{ddagger}, GERALD MC MAHON{ddagger}, JOHANNES WALTENBERGER§, NORBERT F. VOELKEL{dagger},¶ and RUBIN M. TUDER*,¶1

* Department of Pathology,
{dagger} Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA;
{ddagger} SUGEN, Incorporated, South San Francisco, California 94080, USA;
§ Department of Internal Medicine II, Cardiology, Ulm University Medical Center, D-89081, Germany; and
Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA

1Correspondence: Department of Pathology, Campus Box B216, University of Colorado Health Sciences Center, 4200 E. 9th Ave., Denver, CO 80262, USA. E-mail: Rubin.Tuder{at}uchsc.edu

Our understanding of the pathobiology of severe pulmonary hypertension, usually a fatal disease, has been hampered by the lack of information of its natural history. We have demonstrated that, in human severe pulmonary hypertension, the precapillary pulmonary arteries show occlusion by proliferated endothelial cells. Vascular endothelial growth factor (VEGF) and its receptor 2 (VEGFR-2) are involved in proper maintenance, differentiation, and function of endothelial cells. We demonstrate here that VEGFR-2 blockade with SU5416 in combination with chronic hypobaric hypoxia causes severe pulmonary hypertension associated with precapillary arterial occlusion by proliferating endothelial cells. Prior to and concomitant with the development of severe pulmonary hypertension, lungs of chronically hypoxic SU5416-treated rats show significant pulmonary endothelial cell death, as demonstrated by activated caspase 3 immunostaining and TUNEL. The broad caspase inhibitor Z-Asp-CH2-DCB prevents the development of intravascular pulmonary endothelial cell growth and severe pulmonary hypertension caused by the combination of SU5416 and chronic hypoxia.—Taraseviciene-Stewart, L., Kasahara, Y., Alger, L., Hirth, P., McMahon, G., Waltenberger, J., Voelkel, N. F., Tuder, R. M. Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death-dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension.


Key Words: apoptosis • survival • selection • pulmonary vascular remodeling • angiogenesis




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