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Primary Pulmonary Hypertension Between Inflammation and Cancer FREE TO VIEW

Norbert F. Voelkel; Carlyne Cool; S. D. Lee; L. Wright; Mark W. Geraci; Rubin M. Tuder
Author and Funding Information

From the Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver

Norbert Voelkel, University of Colorado Health Science Ctr, Box C-272, Denver, CO 80262

1998 by the American College of Chest Physicians

Chest. 1998;114(3_Supplement):225S-230S. doi:10.1378/chest.114.3_Supplement.225S
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We believe that the monoclonal cell expansion in primary pulmonary hypertension is the result of autonomous growth of stem cell-like endothelial cells, whereas the polyclonal proliferation in secondary pulmonary hypertension occurs as a response of endothelial cells to exogenous stimuli (like viral infection or high shear stress). In this context, we propose that different transcriptional and translational events govern the growth and expansion of monoclonal when compared with polyclonal pulmonary endothelial cells. The availability of antibodies directed against specific tyrosine kinase proteins involved in vasculogenesis/angiogenesis now permits the identification and localization of the components of such a misguided angiogenesis cell proliferation program in the pulmonary hypertensive vascular lesions.




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