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 vital 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.
|Original language||English (US)|
|Issue number||3 SUPPL.|
|State||Published - Jan 1 1998|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine