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 …