DOI QR코드

DOI QR Code

The Relationship of Pulmonary Artery Copper Concentrations and Genes Involved in Copper Homeostasis in Cattle, Swine, and Goats

  • Han, Hyung-Chul (Department of Animal Sciences, Colorado State University) ;
  • So, Hye-Jin (Department of Animal Sciences, Colorado State University) ;
  • Domby, Elizabeth (Department of Animal Sciences, Colorado State University) ;
  • Engle, Terry (Department of Animal Sciences, Colorado State University)
  • Received : 2011.06.25
  • Accepted : 2011.08.17
  • Published : 2012.02.01

Abstract

Liver and pulmonary artery tissue from 5 Angus cross bred steers, 6 goats, and 6 pigs were collected at a commercial abattoir to examine the relationship of pulmonary artery copper (Cu) concentrations and genes involved in copper homeostasis. Liver and pulmonary artery samples were collected at the time of harvest and snap frozen. Liver and pulmonary artery Cu concentrations were determined via flame atomic absorption spectrophotometry and gene expression was determined via real time PCR. Liver Cu concentrations (mg Cu/kg DM${\pm}$SE) were higher (p<0.01) in cows ($396.4{\pm}109.1$) and goats ($181.4{\pm}37.0$) than in pigs ($19.2{\pm}3.5$). All liver Cu concentrations were within normal ranges and considered adequate for each species. Liver Cu concentration was more variable in cows and goats compared to pig liver Cu concentrations. Pulmonary artery ${\beta}$-hydroxylproline was higher (p<0.01) in cow and pig than goat. Real Time PCR revealed that goat liver atp7a was positively correlated ($r^2$ = 0.92; p<0.01) to liver Cu concentrations while cow and pig atp7a was not correlated to liver Cu concentration. In the pig, liver atp7a concentration was positively correlated to atp7b ($r^2$ = 0.66; p<0.05). Pulmonary artery Cu concentration was highest in cows ($14.9{\pm}4.7$), intermediate in pigs ($8.9{\pm}3.3$), and lowest in goats ($3.9{\pm}1.1$). Goat pulmonary artery Cu concentration was not correlated to ctr1 concentration, however, atp7a concentration was positively correlated with ctr1 ($r^2$ = 0.90; p<0.01). In cow pulmonary artery, loxl1 concentration was positively correlated to eln mRNA concentration ($r^2$ = 0.91; p<0.02). Pulmonary artery CTR1 protein concentration was positively correlated to pulmonary artery Cu ($r^2$ = 0.85; p = 0.03) concentration while negatively correlated to liver Cu ($r^2$ = -0.79; p<0.04). Pulmonary artery Cu concentration was not correlated to concentration of Cu homeostatic genes in the pig. These data indicate that genes involved in Cu homeostasis (ctr1, atp7A, atp7B, loxl1 and eln) are differently regulated in different species.

Keywords

References

  1. Bennetts, H. W. and H. T. Hall. 1939. "Falling Disease" of cattle in the south-west of western Australia. Aust. Vet. J. 15:152-159. https://doi.org/10.1111/j.1751-0813.1939.tb01225.x
  2. Borel, A., D. Eichenberger, J. Farjanel, E. Kessler, C. Gleyzal, D. J. Hulmes, P. Sommer and B. Font. 2001. Lysyl oxidase-like protein from bovine aorta. Isolation and maturation to an active form by bone morphogenetic protein-1. J. Biol. Chem. 276:48944-48949. https://doi.org/10.1074/jbc.M109499200
  3. Dargatz, D. A., F. B. Garry, G. B. Clark and P. F. Ross. 1999. Serum copper concentrations in beef cows and heifers. J. Am. Vet. Med. Assoc. 215:1828-1832.
  4. Guentner, H. P., H. R. Lenzinger and M. Doder. 1976. Clinical aspects of the sick sinus syndrome. Springer-Verlag, New York.
  5. Han, H., S. L. Archibeque and T. E. Engle. 2009. Characterization and identification of hepatic mRNA related to copper metabolism and homeostasis in cattle. Biol. Trace Elem. Res. 129:130-136. https://doi.org/10.1007/s12011-008-8293-6
  6. Han, H., T. R. Hansen, B. Berg, B. W. Hess and S. P. Ford. 2008. Maternal undernutrition induces differential cardiac gene expression in pulmonary hypertensive steers at high elevation. Am. J. Physiol. Heart Circ. Physiol. 295:H382-389. https://doi.org/10.1152/ajpheart.01272.2007
  7. Harris, E. D. 1976. Copper-induced activation of aortic lysyl oxidase in vivo. Proc. Natl. Acad. Sci. USA 73:371-374. https://doi.org/10.1073/pnas.73.2.371
  8. Holmberg, C. G. and C. B. Laurell. 1947. Investigations in serum copper; nature of serum copper and its relation to the iron-binding protein in human serum. Acta Chem. Scand. 1:944-950. https://doi.org/10.3891/acta.chem.scand.01-0944
  9. Holmberg, C. G. and C. B. Laurell. 1948. Histaminolytic activity of a copper protein in serum. Nature 161:236.
  10. Kepler, C. R., W. P. Tucker and S. B. Tove. 1971. Biohydrogenation of unsaturated fatty acids. V. Stereospecificity of proton addition and mechanism of action of linoleic acid delta 12-cis, delta 11-trans-isomerase from Butyrivibrio fibrisolvens. J. Biol. Chem. 246:2765-2771.
  11. Kuo, Y. M., B. Zhou, D. Cosco and J. Gitschier. 2001. The copper transporter CTR1 provides an essential function in mammalian embryonic development. Proc. Natl. Acad. Sci. USA 98:6836-6841. https://doi.org/10.1073/pnas.111057298
  12. Liu, X., Y. Zhao, J. Gao, B. Pawlyk, B. Starcher, J. A. Spencer, H. Yanagisawa, J. Zuo and T. Li. 2004. Elastic fiber homeostasis requires lysyl oxidase-like 1 protein. Nat. Genet. 36:178-182. https://doi.org/10.1038/ng1297
  13. Lucero, H. A. and H. M. Kagan. 2006. Lysyl oxidase: an oxidative enzyme and effector of cell function. Cell. Mol. Life Sci. 63:2304-2316. https://doi.org/10.1007/s00018-006-6149-9
  14. Maki, J. M. 2009. Lysyl oxidases in mammalian development and certain pathological conditions. Histol. Histopathol 24:651-660.
  15. O'Dell, B. L., B. C. Hardwich, G. Reynolds and J. E. Savage. 1961. Connective tissue defect in the chick resulting from copper deficiency. In: Proc. Soc. Exp. Biol. Med. p. 402.
  16. Ooshima, A. and O. Midorikawa. 1977. Increased lysyl oxidase activity in blood vessels of hypertensive rats and effect of beta-aminopropionitrile on arteriosclerosis. Jpn. Circ. J. 41:1337-1340.
  17. Pena, M. M., J. Lee and D. J. Thiele. 1999. A delicate balance: homeostatic control of copper uptake and distribution. J. Nutr. 129: 1251-1260.
  18. Prohaska, J. R. and A. A. Gybina. 2004. Intracellular copper transport in mammals. J. Nutr. 134:1003-1006.
  19. Rhodes, J. 2005. Comparative physiology of hypoxic pulmonary hypertension: historical clues from brisket disease. J. Appl. Physiol. 98:1092-1100.
  20. Shields, G. S., W. F. Coulson, D. A. Kimbell, G. E. Cartwright and M. Winthrobe. 1962. Studies on copper metabolism XXXII. Cardiovascular lesions in copper deficient swine. Am. J. Pathol. 41:603-621.
  21. Siegel, R. C., S. R. Pinnell and G. R. Martin. 1970. Cross-linking of collagen and elastin. Properties of lysyl oxidase. Biochemistry 9:4486-4492. https://doi.org/10.1021/bi00825a004
  22. Spears, J. W. 2003. Trace mineral bioavailability in ruminants. J. Nutr. 133:1506S-1509S.
  23. Stenmark, K. R., J. Fasules, D. M. Hyde, N. F. Voelkel, J. Henson, A. Tucker, H. Wilson and J. T. Reeves. 1987. Severe pulmonary hypertension and arterial adventitial changes in newborn calves at 4,300 m. J. Appl. Physiol. 62:821-830.
  24. Sun, R., Y. Yan, X. Chen, Q. Si and H. Li. 1994. Role of collagen metabolism changes in the pathogenesis of pulmonary hypertension in rats and its reversibility. Chin. Med. Sci. J. 9: 183-186.
  25. Switzer, B. R. and G. K. Summer. 1971. Improved method for hydroxyproline analysis in tissue hydrolyzates. Anal. Biochem. 39:487-491. https://doi.org/10.1016/0003-2697(71)90438-6
  26. Tozzi, C. A., D. L. Christiansen, G. J. Poiani and D. J. Riley. 1994. Excess collagen in hypertensive pulmonary arteries decreases vascular distensibility. Am. J. Respir. Crit. Care Med. 149: 1317-1326. https://doi.org/10.1164/ajrccm.149.5.8173773
  27. Wapnir, R. A. 1998. Copper absorption and bioavailability. Am. J. Clin. Nutr. 67:1054S-1060S.
  28. Zoubek, G. L., E. R. Peo, Jr., B. D. Moser, T. Stahly and P. J. Cunningham. 1975. Effects of source on copper uptake by swine. J. Anim. Sci. 40:880-884.

Cited by

  1. In situ and in vitro estimation of mineral release from common feedstuffs fed to cattle vol.155, pp.7, 2012, https://doi.org/10.1017/s002185961700034x