Role of stretch on tight junction structure in alveolar epithelial cells.

摘要: Previous studies have demonstrated that high tidal volumes can cause interstitial and alveolar edema, with degradation of pulmonary epithelial barrier integrity. Separate shown F-actin disruption decreased intracellular ATP (ATP(i)) levels in the nonpulmonary epithelium increase tight junction (TJ) permeability. We hypothesized large stretch perturbs ATP(i) actin architecture, each which adversely affects TJ structure, thus increases Primary cells were subjected to a uniform 25% or 37% change surface area (DeltaSA), cyclic biaxial (15 cycles/min) for 1 h, treated either glycolytic metabolic inhibitors cytoskeletal disrupting agents. Unstretched, untreated served as controls. Changes proteins occludin ZO-1 determined by immunocytochemical evaluation. A amplitude DeltaSA did not produce any significant cytologic changes compared controls, but an resulted decreases intensity peripheral band, degree cell-cell attachment (CCA), total cellular content. depletion significantly diminished band CCA. Actin affect protein intensities (although distribution became punctate) altered Untreated stretched cyclically at 50% h had unstretched These results suggest stretch-induced reduction perturbation disrupt structure CCA, may lead flooding associated volumes.