title: Changes in elastin, elastin binding protein and versican in alveoli in chronic obstructive pulmonary disease.
abstract: BACKGROUND
  COPD is characterised by loss of alveolar elastic fibers and by lack of effective repair. Elastic fibers are assembled at cell surfaces by elastin binding protein (EBP), a molecular chaperone whose function can be reversibility inhibited by chondroitin sulphate of matrix proteoglycans such as versican. This study aimed to determine if alveoli of patients with mild to moderate COPD contained increased amounts of versican and a corresponding decrease in EBP, and if these changes were correlated with decreases in elastin and FEV1.
  
  
  METHODS
  Lung samples were obtained from 26 control (FEV1 > or = 80% predicted, FEV1/VC >0.7) and 17 COPD patients (FEV1 > or = 40% - <80% predicted, FEV1/VC < or = 0.7) who had undergone a lobectomy for bronchial carcinoma. Samples were processed for histological and immuno-staining. Volume fractions (Vv) of elastin in alveolar walls and alveolar rims were determined by point counting, and versican and EBP assessed by grading of staining intensities.
  
  
  RESULTS
  Elastin Vv was positively correlated with FEV1 for both the alveolar walls (r = 0.66, p < 0.001) and rims (r = 0.41, p < 0.01). Versican was negatively correlated with FEV1 in both regions (r = 0.30 and 0.32 respectively, p < 0.05), with the highest staining intensities found in patients with the lowest values for FEV1. Conversely, staining intensities for EBP in alveolar walls and rims and were positively correlated with FEV1 (r = 0.43 and 0.46, p < 0.01).
  
  
  CONCLUSIONS
  Patients with mild to moderate COPD show progressively increased immuno-staining for versican and correspondingly decreased immuno-staining for EBP, with decreasing values of FEV1. These findings may explain the lack of repair of elastic fibers in the lungs of patients with moderate COPD. Removal of versican may offer a strategy for effective repair.
authors.affiliation: Department of Anatomy with Radiology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand. m.merrilees@auckland.ac.nz
authors.forename: Mervyn J
authors.initials: MJ
authors.lastname: Merrilees
authors.forename: Pamela S T
authors.initials: PS
authors.lastname: Ching
authors.forename: Brent
authors.initials: B
authors.lastname: Beaumont
authors.forename: Aleksander
authors.initials: A
authors.lastname: Hinek
authors.forename: Thomas N
authors.initials: TN
authors.lastname: Wight
authors.forename: Peter N
authors.initials: PN
authors.lastname: Black
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D004549:Elastin / Q000378:metabolism*; D005541:Forced Expiratory Volume; D006801:Humans; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000378:metabolism*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*; D012720:Severity of Illness Index; D053675:Versicans / Q000378:metabolism*
chemical_list: D011956:Receptors, Cell Surface; C054901:elastin-binding proteins; D053675:Versicans; D004549:Elastin