title: Heaves, an asthma-like equine disease, involves airway smooth muscle remodeling.
abstract: BACKGROUND
  Increased airway smooth muscle mass is a prominent feature of asthmatic airway remodeling. Airway smooth muscle hyperplasia occurs in rodent models of experimental asthma, but the relevance of such finding to spontaneously occurring disease in large mammals is unknown.
  
  
  OBJECTIVE
  We examined horses with heaves, a naturally occurring equine asthma related to sensitization and exposure to moldy hay. We hypothesized that airway remodeling occurs in heaves and shares disease mechanisms with asthma.
  
  
  METHODS
  We quantified the airway smooth muscle mass and the numbers of proliferating and apoptotic airway smooth muscle cells in 5 horses with heaves and 5 control horses using morphometric techniques. Cell proliferation was detected in tissue sections by immunostaining for proliferating cell nuclear antigen, and apoptotic cells were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling of fragmented DNA. Both signals were colocalized with smooth muscle specific alpha-actin.
  
  
  RESULTS
  Horses with heaves had a significant increase in the amount of smooth muscle in the airways (nearly triple that of the controls) associated with increased myocyte proliferation (7-fold proliferating cell nuclear antigen-positive airway myocytes) and apoptosis (6-fold).
  
  
  CONCLUSIONS
  Heaves involves airway smooth muscle growth associated with myocyte hyperplasia, which may contribute to the growth, and increased myocyte apoptosis that may reflect a compensatory mechanism serving to limit the abnormal smooth muscle growth.
  
  
  CONCLUSIONS
  Airway smooth muscle remodeling in heaves may be involved in the mechanism of airway hyperresponsiveness and chronic lung function impairment in a way comparable to human asthma.
authors.affiliation: Meakins-Christie Laboratories, McGill University, 3626 Saint Urbain, Montreal, Quebec H2X 2P2, Canada.
authors.forename: Bérénice
authors.initials: B
authors.lastname: Herszberg
authors.forename: David
authors.initials: D
authors.lastname: Ramos-Barbón
authors.forename: Meiyo
authors.initials: M
authors.lastname: Tamaoka
authors.forename: James G
authors.initials: JG
authors.lastname: Martin
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Lavoie
mesh_terms: D000818:Animals; D017209:Apoptosis; D001249:Asthma / Q000276:immunology / Q000473:pathology* / Q000662:veterinary*; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D049109:Cell Proliferation; D004195:Disease Models, Animal; D005260:Female; D006734:Horse Diseases / Q000276:immunology / Q000473:pathology*; D006736:Horses; D008297:Male; D032342:Muscle Cells / Q000276:immunology / Q000473:pathology; D009130:Muscle, Smooth / Q000276:immunology / Q000473:pathology*; D018809:Proliferating Cell Nuclear Antigen / Q000276:immunology
chemical_list: D018809:Proliferating Cell Nuclear Antigen