Abstract
Dramatic fibroproliferative changes in the adventitia of pulmonary arteries (PAs) have been observed in humans and animal models of chronic hypoxic pulmonary hypertension. We have shown that proliferation and apoptosis contribute to this remodeling response. We tested the hypothesis that hypoxia, in the absence of exogenous comitogens, acts directly on PA adventitial fibroblasts to induce proliferation and apoptosis and that the responses are dependent on differential activation of mitogen-activated protein (MAP) kinase family members.
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