Chronic hypoxic pulmonary hypertension, especially in the young, is characterized by striking fibroproliferative changes in the adventitia of both large and small pulmonary arteries. These changes are thought to contribute significantly to high pulmonary vascular resistance and, in some instances, to cor pulmonale. It has long been assumed that the resident pulmonary artery fibroblasts are the primary contributors to adventitial thickening and fibrosis. However, there is evidence that circulating mononuclear cells of a myeloid origin, which have the capability of exhibiting fibroblast-like properties, can be chemotactically recruited to sites of tissue injury and participate in the repair process.1– In fact, bone marrow-derived fibroblast precursor cells have recently been suggested2– to be major contributors to lung fibrosis following bleomycin-induced injury. However, whether circulating precursor cells with the potential to exhibit fibroblast-like properties contribute to adventitial thickening under hypoxic conditions is unknown. We recently demonstrated3 the presence of hematopoietic precursor cells expressing cKit marker in the adventitia of chronically hypoxic animals. We therefore tested the hypothesis that, in hypoxia-induced pulmonary hypertension, circulating mononuclear cells contribute to pulmonary artery adventitial thickening and fibrosis.