PRIMARY PULMONARY-HYPERTENSION BETWEEN INFLAMMATION AND CANCER

We believe that the monoclonal cell expansion in primary pulmonary hyp ertension is the result of autonomous growth of stem cell-like endothe lial cells, whereas the polyclonal proliferation in secondary pulmonar y 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 gov ern the growth and expansion of monoclonal when compared with polyclon al pulmonary endothelial cells. The availability of antibodies directe d against specific tyrosine kinase proteins involved in vasculogenesis /angiogenesis now permits the identification and localization of the c omponents of such a misguided angiogenesis cell proliferation program in the pulmonary hypertensive vascular lesions.