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Plasticity of vascular progenitor cells: Implications in pulmonary vascular remodelling in COPD

Depts of Pulmonary Medicine and Pathology, Idibaps-Hospital Clinic, University of Barcelona, Barcelona, Spain

CORRESPONDENCE: Marta Díez, Physiological Mechanisms of Respiratory Diseases Laboratory, IDIBAPS, Hospital Clinic de Barcelona, Barcelona, Spain

Vascular progenitor cells (VPC) have shown in vitro and in vivo their ability to differentiate into endothelial cells (EC). Some evidence suggests that the plasticity of these cells to differentiate into other cell types might contribute not only to angiogenesis but also to perpetuate vascular lesions. Studies done in pulmonary arteries (PA) of patients with COPD have demonstrated the presence of VPC infiltrating the intima. Since intimal thickening is mainly constituted by smooth muscle cells (SMC), we asked whether VPC could play a role in wall thickening. Accordingly, the objective was to evaluate in vitro the plasticity of VPC to differentiate into SMC and EC of human PA. G-CSF-mobilized peripheral blood CD133+ cells from a commercial primary line were expanded and labelled with acetylated-LDL-DiI for tracking cell purposes. Then, cells were co-cultured with commercial primary lines of human PA EC or SMC (n = 3). As control, CD133+ cells were cultured alone, with minimal medium with or without VEGF (50ng·ml^–1). After 6 and 12 days of growth, the phenotype of cultures was characterized by immunofluorescence with: lectin, -actin and CD31. Cells were also evaluated morphologically. After 6 days, VPC acquired the morphology and the phenotype of the cells with which they were co-cultured, EC (lectin+, CD31+, -actin-) or SMC (-actin+, lectin-, CD31-). VPC cultured 12 days alone or with VEGF did not acquire typical morphology and markers of mature EC or SMC of PA. We conclude that VPC have the potential to differentiate in vitro into SMC, and that this plasticity could contribute to perpetuate pulmonary vascular remodelling in COPD.