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Use of western immunoblot for evaluation of myocardial dystrophin, α-sarcoglycan, and β-dystroglycan in dogs with idiopathic dilated cardiomyopathy

Alan W SpierDepartments of Veterinary Clinical Sciences, College of Veterinary Medicine.

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Kathryn M. MeursDepartments of Veterinary Clinical Sciences, College of Veterinary Medicine.

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 DVM, PhD
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Daniel D CoovertMolecular and Cellular Biochemistry, College of Medicine and Public Health.

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Linda B. LehmkuhlDepartments of Veterinary Clinical Sciences, College of Veterinary Medicine.

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Michael R. O'GradyThe Ohio State University, Columbus, OH, 43210; the Department of Clinical Sciences, Ontario Veterinary College Guelph, Ontario, Canada N1G 2W1 .

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Lisa M. FreemanDepartment of Clinical Sciences, College of Veterinary Medicine, Tufts University, North Grafton, MA 01536 .

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Arthur H. BurghesMolecular and Cellular Biochemistry, College of Medicine and Public Health.

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Jeffrey A. TowbinDepartment of Pediatrics (Cardiology Section), Baylor College of Medicine, Houston, TX 77030.

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Abstract

Objective—To evaluate the potential importance of dystrophin, α-sarcoglycan (adhalin), and β-dystroglycan, by use of western blot analysis, in several breeds of dogs with dilated cardiomyopathy.

Sample Population—Myocardial samples obtained from 12 dogs were evaluated, including tissues from 7 dogs affected with dilated cardiomyopathy, 4 control dogs with no identifiable heart disease (positive control), and 1 dog affected with Duchenne muscular dystrophy (negative control for dystrophin). Of the affected dogs, 4 breeds were represented (Doberman Pinscher, Dalmatian, Bullmastiff, and Irish Wolfhound).

Procedure—Western blot analysis was used for evaluation of myocardial samples obtained from dogs with and without dilated cardiomyopathy for the presence of dystrophin and 2 of its associated glycoproteins, α-sarcoglycan and β-dystroglycan.

Results—Detectable differences were not identified between dogs with and without myocardial disease in any of the proteins evaluated.

Conclusions and Clinical Relevance—Abnormalities in dystrophin, α-sarcoglycan, and β-dystroglycan proteins were not associated with the development of dilated cardiomyopathy in the dogs evaluated in this study. In humans, the development of molecular biological techniques has allowed for the identification of specific causes of dilated cardiomyopathy that were once considered to be idiopathic. The use of similar techniques in veterinary medicine may aid in the identification of the cause of idiopathic dilated cardiomyopathy in dogs, and may offer new avenues for therapeutic intervention. ( Am J Vet Res 2001;62:67–71)

Abstract

Objective—To evaluate the potential importance of dystrophin, α-sarcoglycan (adhalin), and β-dystroglycan, by use of western blot analysis, in several breeds of dogs with dilated cardiomyopathy.

Sample Population—Myocardial samples obtained from 12 dogs were evaluated, including tissues from 7 dogs affected with dilated cardiomyopathy, 4 control dogs with no identifiable heart disease (positive control), and 1 dog affected with Duchenne muscular dystrophy (negative control for dystrophin). Of the affected dogs, 4 breeds were represented (Doberman Pinscher, Dalmatian, Bullmastiff, and Irish Wolfhound).

Procedure—Western blot analysis was used for evaluation of myocardial samples obtained from dogs with and without dilated cardiomyopathy for the presence of dystrophin and 2 of its associated glycoproteins, α-sarcoglycan and β-dystroglycan.

Results—Detectable differences were not identified between dogs with and without myocardial disease in any of the proteins evaluated.

Conclusions and Clinical Relevance—Abnormalities in dystrophin, α-sarcoglycan, and β-dystroglycan proteins were not associated with the development of dilated cardiomyopathy in the dogs evaluated in this study. In humans, the development of molecular biological techniques has allowed for the identification of specific causes of dilated cardiomyopathy that were once considered to be idiopathic. The use of similar techniques in veterinary medicine may aid in the identification of the cause of idiopathic dilated cardiomyopathy in dogs, and may offer new avenues for therapeutic intervention. ( Am J Vet Res 2001;62:67–71)