Procaterol inhibits lung fibroblast migration

Fibroblasts are important cells that are involved in modulation of fibrosis after injuries. In some uncontrollable inflammatory processes, excess fibroblasts migrate around the small airway. The pathogenesis of chronic obstructive pulmonary disease is related to fibrosis around the small airways. The aim of the current study was to investigate the effect of procaterol, a second-generation beta (2)-agonist, on migration of human fetal lung fibroblasts (HFL-1) induced by human plasma fibronectin (HFn). Using the blindwell chamber technique, 10(-8) M procaterol inhibited migration of HFL-1 (control, 100%; 10(-8) M, 73.2 +/- 4.9%; n = 6, p < 0.05). The inhibitory effect of procaterol was concentration-dependent. Although a beta 2-receptor inhibitor, ICI 181551, blocked the inhibitory effect of procaterol, a beta 1-receptor inhibitor, atenolol, did not. Because a cyclic AMP-dependent protein kinase (PKA) inhibitor, KT5720, blocked the effect of procaterol, the cyclic AMP-PKA pathway may be involved in the migration inhibitory process. Procaterol, which is prescribed mainly for treatment of bronchial asthma, might be a useful drug for inhibiting lung fibrosis following injuries to the lung.