The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Janus face of vascular endothelial growth factor: the obligatory survival factor for lung vascular endothelium controls precapillary artery remodeling in severe pulmonary hypertension.
Norbert F Voelkel; Carlyne Cool; Laima Taraceviene-Stewart; Mark W Geraci; Michael Yeager; Todd Bull; Michael Kasper; Rubin M Tuder (Profiled Author: Rubin Tuder)
University of Colorado Health Sciences Center, Denver, CO 80262, USA. email@example.com
Critical care medicine 2002;30(5 Suppl):S251-6.
Vascular endothelial growth factor (VEGF) plays a central role in the life and death of pulmonary vascular endothelial cells. Treatment of neonatal or adult rats with a VEGF receptor blocker destroys lung capillaries by inducing endothelial cell apoptosis and causes emphysema. Human lung tissue samples from patients with endstage emphysema have decreased levels of VEGF messenger RNA and protein and have decreased expression of kinase insert domain-containing receptor (VEGF receptor II). These decreases are associated with a high rate of alveolar septal cell apoptosis, indicating perhaps that decreased VEGF and kinase insert domain-containing receptor expression impairs endothelial cell survival in emphysematous lungs. Combination of VEGF receptor blockade with chronic hypoxia (3-wk exposure) results in obliteration of small precapillary pulmonary arteries by proliferating endothelial cells, severe pulmonary hypertension, and death caused by right-side heart failure. We propose that 1) VEGF receptor blockade causes endothelial cell apoptosis, 2) hypoxic vasoconstriction (shear stress) selects apoptosis-resistant endothelial cells that proliferate and obliterate the lumen, and 3) the vascular remodeling observed is relevant to the structural alterations that characterize severe pulmonary hypertension (including primary pulmonary hypertension) in humans. The endovascular cell growth in human disease and in our model exhibits some similarities with neoplastic cell growth. Chemotherapy strategies can now be employed in the animal model in an attempt to treat established vascular-obliterative lung disease.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
C D Cool; J S Stewart; P Werahera; G J Miller; R L Williams; N F Voelkel; R M Tuder
Three-dimensional reconstruction of pulmonary arteries in plexiform pulmonary hypertension using cell-specific markers. Evidence for a dynamic and heterogeneous process of pulmonary endothelial cell growth.The American journal of pathology 1999;155(2):411-9.
P M Becker; A D Verin; M A Booth; F Liu; A Birukova; J G GarciaAmerican journal of physiology. Lung cellular and molecular physiology 2001;281(6):L1500-11.
R M Tuder; M Chacon; L Alger; J Wang; L Taraseviciene-Stewart; Y Kasahara; C D Cool; A E Bishop; M Geraci; G L Semenza; et al.The Journal of pathology 2001;195(3):367-74.
Appears in this Publication
Author of this Publication