Journal Article

The pigeon (<i>Columba livia</i>) model of spontaneous atherosclerosis

J. L. Anderson, S. C. Smith and R. L. Taylor

in Poultry Science

Volume 93, issue 11, pages 2691-2699
Published in print November 2014 | ISSN: 0032-5791
Published online November 2014 | e-ISSN: 1525-3171 | DOI: https://dx.doi.org/10.3382/ps.2014-04280
The pigeon (Columba livia) model of spontaneous atherosclerosis

More Like This

Show all results sharing these subjects:

  • Zoology and Animal Sciences
  • Animal Pathology and Diseases
  • Animal Physiology
  • Ornithology
  • Veterinary Medicine

GO

Show Summary Details

Preview

Multiple animal models have been employed to study human atherosclerosis, the principal cause of mortality in the United States. Each model has individual advantages related to specific pathologies. Initiation, the earliest disease phase, is best modeled by the White Carneau (WC-As) pigeon. Atherosclerosis develops spontaneously in the WC-As without either external manipulation or known risk factors. Furthermore, susceptibility is caused by a single gene defect inherited in an autosomal recessive manner. The Show Racer (SR-Ar) pigeon is resistant to atherosclerosis. Breed differences in the biochemistry and metabolism of celiac foci cells have been described. For example, WC-As have lower oxidative metabolism but higher amounts of chondroitin-6-sulfate and nonesterified fatty acids compared with SR-Ar. Gene expression in aortic smooth muscle cells was compared between breeds using representational difference analysis and microarray analysis. Energy metabolism and cellular phenotype were the chief gene expression differences. Glycolysis and synthetic cell types were related to the WC-As but oxidative metabolism and contractile cell types were related to the SR-Ar. Rosiglitazone, a PPARγ agonist, blocked RNA binding motif (RBMS1) expression in WC-As cells. The drug may act through the c-myc oncogene as RBMS1 is a c-myc target. Proteomic tests of aortic smooth muscle cells supported greater glycosylation in the WC-As and a transforming growth factor β effect in SR-Ar. Unoxidized fatty acids build up in WC-As cells because of their metabolic deficiency, ultimately preventing the contractile phenotype in these cells. The single gene responsible for the disease is likely regulatory in nature.

Keywords: genetics; oxidative metabolism; glycolysis; contractile phenotype; synthetic phenotype

Journal Article.  7179 words. 

Subjects: Zoology and Animal Sciences ; Animal Pathology and Diseases ; Animal Physiology ; Ornithology ; Veterinary Medicine

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.