title: Evaluation of the genes encoding CD39/NTPDase-1 and CD39L1/NTPDase-2 in horses with and without abnormal hemorrhage and in horses with pathologic evidence of exercise-induced pulmonary hemorrhage.
abstract: BACKGROUND
  Exercise-induced pulmonary hemorrhage (EIPH) is a common disorder of equine athletes. The role of polymorphisms in genes encoding hemostasis-regulatory proteins in horses with abnormal hemorrhage is unknown.
  
  
  OBJECTIVE
  The goal of this study was to evaluate the genes encoding 2 ectonucleotidases, CD39/NTPDase-1 and CD39L1/NTPDase-2, and one ecto-5' nucleotidase, CD73, in horses with abnormal hemorrhage or pathologic changes consistent with EIPH.
  
  
  METHODS
  Twenty-three horses with histories of abnormal hemorrhage, 8 horses with gastrointestinal signs, and 45 healthy horses were evaluated using polymerase chain reaction-based techniques. Formalin-fixed tissues from 21 horses with pathologic changes consistent with EIPH were also evaluated.
  
  
  RESULTS
  Three single nucleotide polymorphisms (SNPs) were identified in the gene encoding CD39 and one SNP was identified in the gene encoding CD39L1. No SNPs were identified in the gene encoding CD73. CD39 SNPs were identified in 19 of 20 (95%) horses with unexplained hemorrhage and 20 of 21 (95%) horses with pathologic features consistent with EIPH. CD39L1 SNPs were identified in 6 of 20 (30%) horses with unexplained hemorrhage and 8 of 21 (38%) horses with pathologic features consistent with EIPH. CD39 and CD39L1 SNPs were identified in 5 of 8 (62.5%) and one of 8 (12.5%) horses, respectively, presenting with colic or weight loss. CD39 and CD39L1 SNPs were identified in 28 of 45 (62%) and 13 of 45 (28.8%) healthy horses, respectively.
  
  
  CONCLUSIONS
  CD39 and CD39L1 are critically important in maintaining normal hemostasis and limiting inflammation. Further studies are needed to evaluate their role in the pathogenesis of equine EIPH.
authors.affiliation: Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL, USA.
authors.forename: Mary K
authors.initials: MK
authors.lastname: Boudreaux
authors.affiliation: Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL, USA.
authors.forename: Jennifer
authors.initials: J
authors.lastname: Koehler
authors.affiliation: Department of Pathobiology, New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
authors.forename: Perry L
authors.initials: PL
authors.lastname: Habecker
authors.affiliation: Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, USA.
authors.forename: Fabio
authors.initials: F
authors.lastname: Del Piero
mesh_terms: D000251:Adenosine Triphosphatases / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D001081:Apyrase / Q000235:genetics / Q000378:metabolism*; D015971:Gene Expression Regulation, Enzymologic; D020022:Genetic Predisposition to Disease; D006470:Hemorrhage / Q000235:genetics / Q000378:metabolism / Q000662:veterinary*; D006734:Horse Diseases / Q000235:genetics / Q000378:metabolism*; D006736:Horses; D008171:Lung Diseases / Q000235:genetics / Q000378:metabolism / Q000662:veterinary*; D005082:Physical Exertion; D020641:Polymorphism, Single Nucleotide
chemical_list: D015703:Antigens, CD; D000251:Adenosine Triphosphatases; C027201:ectoATPase; D001081:Apyrase; C067869:CD39 antigen
keywords: Equine; exercise intolerance; molecular; race horses