title: Static stretch induces active morphological remodeling and functional impairment of alveolar epithelial cells.
abstract: BACKGROUND
  Static stretch is frequently observed in the lung. Both static stretch and cyclic stretch can induce cell death and Na(+)/K(+)-ATPase trafficking, but stretch-induced alveolar epithelial cell (AEC) functions are much less responsive to static than to cyclic stretch. AEC remodeling under static stretch may be partly explained.
  
  
  OBJECTIVE
  The aim of this study was to explore the AEC remodeling and functional changes under static stretch conditions.
  
  
  METHODS
  We used A549 cells as a model of AEC type II cells. We assessed F-actin content and cell viability by fluorescence staining at various static-stretch magnitudes and time points. Specifically, we used scanning electron microscopy to explore the possible biological mechanisms used by A549 cells to 'escape' static-stretch-induced injury. Finally, we measured choline cytidylyltransferase-alpha (CCT alpha) mRNA and protein by real-time PCR and Western blot to evaluate cellular secretory function.
  
  
  RESULTS
  The results showed that the magnitude of static stretch was the primary determinant of static-stretch-induced cell death and cytoskeleton organization, but an extended duration of high static deformation/stretch (37% change in surface area) had no cumulative effects on cell death and cytoskeleton organization. AEC remodeling (expansion-contraction-reexpansion) under static stretch conditions may explain this interesting phenomenon partly. After cell remodeling, CCT alpha expression in A549 cells was influenced not only by stretch magnitude but also by stretch time.
  
  
  CONCLUSIONS
  Under static stretch conditions, A549 cells undergo morphological and functional changes. They can survive stress failure from overstretching by remodeling their body to 'escape' the injury. During this complex course of remodeling, cellular function was partly damaged.
authors.affiliation: Beijing Chao-Yang Hospital, Capital Medical University, Beijing Institute of Respiratory Medicine, Beijing, China.
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Ren
authors.forename: Qingyuan
authors.initials: Q
authors.lastname: Zhan
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Hu
authors.forename: Bing
authors.initials: B
authors.lastname: Sun
authors.forename: Chun
authors.initials: C
authors.lastname: Yang
authors.forename: Chen
authors.initials: C
authors.lastname: Wang
mesh_terms: D000199:Actins / Q000378:metabolism; D056809:Alveolar Epithelial Cells / Q000502:physiology*; D015153:Blotting, Western; D045744:Cell Line, Tumor; D048430:Cell Shape; D002470:Cell Survival; D019916:Choline-Phosphate Cytidylyltransferase / Q000378:metabolism; D006801:Humans; D016133:Polymerase Chain Reaction; D013314:Stress, Mechanical
chemical_list: D000199:Actins; D019916:Choline-Phosphate Cytidylyltransferase