INTEGRIN MEDIATION OF TYPE-II CELL ADHERENCE TO PROVISIONAL MATRIX PROTEINS

Lung injury causes alveolar type I epithelial cell death, basement mem brane denudation, and alveolar flooding with serum fibronectin and fib rinogen. For successful restoration of normal architecture, the epithe lium must be regenerated from progenitor type II alveolar cells. Using adhesion assays, we examined whether type II alveolar cells adhere to the provisional matrix proteins fibronectin, fibrinogen, and fibrin, and whether integrins mediate this adherence. Rat type II cells adhere d to fibronectin, vitronectin, fibrinogen, and fibrin. Synthetic RGD ( arginine-glycine-aspartic acid) peptide blocked this adhesion. Flow cy tometry and Western analysis indicated that type II cells expressed be ta(1)- and alpha(v) beta(3)-integrins. Anti-beta(1)- and anti-alpha(v) beta(3)-integrin antibodies blocked type II cell adhesion to fibronec tin and to fibronectin and fibrinogen, respectively. In summary, type II cells adhered to fibronectin, fibrinogen, and fibrin, and adhesion was partially mediated by integrins. This study provides the first evi dence of type II cell adhesion to fibrin gels and vitronectin, beta(1) - and alpha(v) beta(3)-integrin mediation of type II cell adhesion, an d the presence of the alpha(v) beta(3)-integrin on type II epithelial cells.