The contribution of avian models to our understanding of atherosclerosis and their promise for the future

Laboratory Animal Science

Volumn 48, Issue 6, 1998, Pages 565-568

  St Clair, Richard W ^a  

^a WAKE FOREST SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMAL EXPERIMENT; ANIMAL MODEL; ATHEROGENESIS; ATHEROSCLEROSIS; CHICKEN; CONFERENCE PAPER; FOWL; GENETIC SUSCEPTIBILITY; HYPERTENSION; NONHUMAN; PIGEON; QUAIL; TURKEY (BIRD);

ANIMALS; ARTERIOSCLEROSIS; BIRD DISEASES; BIRDS; CHICKENS; COLUMBIDAE; COTURNIX; DISEASE MODELS, ANIMAL; FORECASTING; RESEARCH; TURKEYS;

EID: 0032450780     PISSN: 00236764     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Conference Paper

References (36)

1. Dauber, D. V. 1944. Spontaneous atherosclerosis in chickens. AMA Arch. Path. 38:46-51.
2. Dauber, D. V., and L. N. Katz. 1943. Experimental atherosclerosis in the chick. AMA Arch. Path. 36:473-492.
3. Pick, R., J. Stamler, S. Rodbard, et al. 1952. The inhibition of coronary atherosclerosis by estrogens in cholesterolfed chicks. Circulation 6:276-280.
4. Hajjar, D. P., C. G. Fabricant, C. R. Minick, et al. 1986. Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation. Am. J. Pathol. 122:62-70.
5. Gresham, G. A., and A. N. Howard. 1961. Aortic rupture in the turkey. J. Athero. Res. 1:75-80.
6. Ojerio, A. D., G. J. Pucak, T. B. Clarkson, et al. 1972. Dietinduced atherosclerosis and myocardial infarction in Japanese quail. Lab. Anim. Sci. 22:33-39.
7. Day, C. E., W. W. Stafford, and P. E. Schurr. 1977. Utility of selected line (SEA) of the Japanese quail (Coturnix coturnix japonica) for discovery of new anti-atherosclerosis drugs. Lab. Anim. Sci. 27:817-821.
8. Pyrzak, R., and J. C. H. Shih. 1987. Detection of specific DNA segments of Marek's disease herpes virus in Japanese quail susceptible to atherosclerosis. Atherosclerosis 68:77-85.
9. Shih, J. C. K., E. P. Pullman, and K. J. Kao. 1983. Genetic selection, general characterization, and histology of atherosclerosis-susceptible and -resistant Japanese quail. Atherosclerosis 49:41-53.
10. Clarkson, T. B., R. W. Prichard, M. G. Netsky, et al. 1959. Atherosclerosis in pigeons: its spontaneous occurrence and resemblance to human atherosclerosis. AMA Arch. Pathol. 68:143-147.
11. St. Clair, R. W. 1983. Metabolic changes in the arterial wall associated with atherosclerosis in the pigeon. Fed. Proc. 42:2489-2485.
12. Barakat, H. A., and R. W. St. Clair. 1985. Characterization of plasma lipoproteins of grain- and cholesterol-fed white carneau and show racer pigeons. J. Lipid Res. 26:1252-1268.
13. Randolph, R. K., and R. W. St. Clair. 1984. Pigeon aortic smooth muscle cells lack a functional low density lipoprotein receptor pathway. J. Lipid Res. 25:888-902.
14. St. Clair, R. W., M. A. Leight, and H. A. Barakat. 1986. Metabolism of low density lipoproteins by pigeon skin fibroblasts and aortic smooth muscle cells. Comparisons of cells from atherosclerosis-susceptible and atherosclerosis-resistant pigeons. Arteriosclerosis 6:170-177.
15. Reagan, J. W., Jr., L. R. Miller, and R. W. St. Clair. 1990. In vivo clearance of low density lipoprotein in pigeons occurs by a receptor-like mechanism that is not down-regulated by cholesterol feeding. J. Biol. Chem. 265:9381-9391.
16. Sulistiyani, and R. W. St. Clair. 1991. The method of isolation of primary cells and their subculture influences the expression of LDL receptors on pigeon and chicken embryo cells in culture. Atherosclerosis 91:123-135.
17. St. Clair, R. W., H. B. Lofland, Jr., and T. B. Clarkson, Jr. 1970. Influence of duration of cholesterol feeding on esterification of fatty acids by cell-free preparation of pigeon aorta. Studies on the mechanism of cholesterol esterification. Circ. Res. 27:213-225.
18. St. Clair, R. W. 1983. Atherosclerosis regression in animal models: current concepts of cellular biochemical mechanisms. Prog. Cardiovasc. Dis. 26:109-132.
19. Jerome, W. G., and J. C. Lewis. 1985. Early atherogenesis in white carneau pigeons. II. Ultrastructural and cytochemical observations. Am. J. Pathol. 119:210-222.
20. Taylor, R. G., and J. C. Lewis. 1986. Endothelial cell proliferation and monocyte adhesion to atherosclerotic lesions of White Carneau pigeons. Am. J. Pathol. 125:152-160.
21. Lewis, J. C., R. G. Taylor, and W. G. Jerome. 1985. Foam cell characteristics in coronary arteries and aortas of white carneau pigeons with moderate hypercholesterolemia. Ann. N.Y. Acad. Sci. 454:91-100.
22. Denholm, E. M., and J. C. Lewis. 1987. Monocyte chemoattractants in pigeon aortic atherosclerosis. Am. J. Pathol. 126:464-475.
23. Henson, D. A., R. W. St. Clair, and J. C. Lewis. 1989. β-VLDL and acetylated-LDL binding to pigeon monocyte macrophages. Atherosclerosis 78:47-60.
24. Adelman, S. J., and R. W. St. Clair. 1988. Lipoprotein metabolism by macrophages from atherosclerosis-susceptible white carneau and resistant show racer pigeons. J. Lipid Res. 29:643-656.
25. Adelman, S. J., and R. W. St. Clair. 1989. β-VLDL metabolism by pigeon macrophages. Evidence for two binding sites with different potentials for promoting cholesterol accumulation. Arteriosclerosis 9:673-683.
26. Seo, T., and R. W. St. Clair. 1997. Heparan sulfate proteoglycans mediate internalization and degradation of beta-VLDL and promote cholesterol accumulation by pigeon macrophages. J. Lipid Res. 38:765-779.
27. Yancey, P. G., and R. W. St. Clair. 1992. Cholesterol efflux is defective in macrophages from atherosclerosis-susceptible white carneau pigeons relative to resistant show racer pigeons. Arterioscler. Thromb. 12:1291-1304.
28. Yancey, P. G., and R. W. St. Clair. 1994. Mechanism of the defect in cholesteryl ester clearance from macrophages of atherosclerosis-susceptible white carneau pigeons. J. Lipid Res. 35:2114-2129.
29. Schwenke, D. C., and R. W. St. Clair. 1993. Influx, efflux, and accumulation of LDL in normal arterial areas and atherosclerotic lesions of White Carneau pigeons with naturallyoccurring and cholesterol-aggravated aortic atherosclerosis. Arterioscler. Thromb. 13:1368-1381.
30. 125I-tyramine cellobiose labeled LDL is greater in the atherosclerosis-susceptible region of white carneau pigeon aorta and further enhanced once atherosclerotic lesions develop. Arterioscler. Thromb. 12:446-460.
31. Wagner, W. D., and I. J. Edwards. 1989. Metabolic and structural properties of proteoglycans produced by cultured arterial smooth muscle cells of atherosclerosis-susceptible and - resistant species, p. 109-118. In Fifth Munster Internutionul Arteriosclerosis Syillposiurn, Westdeutscher Verlag CMBH.
32. Edwards, I. J., and W. D. Wagner. 1992. Cell surface heparan sulfate proteoglycan and chondroitin sulfate proteoglycan of arterial smooth muscle cells. Am. J. Pathol. 140:193-205.
33. Nimpf, J., and W. J. Schneider. 1991. Receptor-mediated lipoprotein transport in laying hens. J. Nutr. 121:1471-1474.
34. Lehner, N. D. M., B. C. Bullock, and T. B. Clarkson. 1967. Intranuclear inclusion disease of pigeons. J. Am. Vet. Med. Assoc. 151:939-941.
35. Fabricant, C. G., J. Fabricant, M. M. Litrenta, et al. 1978. Virus-induced atherosclerosis. J. Exp. Med. 148:335-340.
36. Hajjar, D. P., C. G. Fabricant, C. R. Minick CR, et al. 1986. Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation. Am. J. Pathol. 122:62-70.