Skip to main content

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 469))

Abstract

Diabetes is strongly associated with an accelerated rate of development of atherosclerosis1. Evidence suggests that elevated serum glucose levels may contribute to atherogenesis in diabetic patients by promoting oxidation of lipoproteins, propagation of free radicals, and production of advanced glycation end-products (AGE)2 3 4. However, the exact mechanisms of how hyperglycemia accelerates atherogenesis are not understood.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Steiner G. 1985. Atherosclerosis, the major complication of diabetes. Adv Exp Med Biol. 189:277–297.

    PubMed  CAS  Google Scholar 

  2. Kawamura M, Heinecke JW, and Cahit A. 1994. Pathophysiological concentrations of glucose promote oxidative modification of LDL by a superoxide-dependent pathway. J Clin Invest. 94: 771–778.

    Article  PubMed  CAS  Google Scholar 

  3. Bellomo G, Maggi E, Poli M, Agosta FG, Bollati P, and Finardi G. 1995. Autoantibodies against oxidatively modified LDL in NIDDM. Diabetes. 44:60–66.

    Article  PubMed  CAS  Google Scholar 

  4. Knecht KJ, Dunn JA, McFarland KF, McCance DR, Lyons TJ, Thorpe SR, and Baynes JW. 1991. Effect of diabetes and aging on carboxymemyllysine levels in human urine. Diabetes. 40:190–196.

    Article  PubMed  CAS  Google Scholar 

  5. Berliner JA, Territo MC, Sevanian A, Ramin S, Kim JA, Barnshad B, Esterson M, and Fogelman AM. 1990. Minimally modified LDL stimulates monocyte:endothelial interactions. J Clin Invest. 85:1260–1266.

    Article  PubMed  CAS  Google Scholar 

  6. Cushing S, Berliner JA, Valente AJ, Territo MC, Navab M, Parhami F, Gerrity R, Schwartz CJ, and Fogelman AM. 1990. Minimally-modified LDL induces monocyte chemotactic protein-1 in human endothelial cells and smooth muscle cells. Proc Natl Acad Sci USA. 87:5134–5138.

    Article  PubMed  CAS  Google Scholar 

  7. Roy P, Roy SK, Mitra A, and Kulkarni AP. 1994. Superoxide generation by LO in the presence of NADH and NADPH. Biochem Biophys Acta. 1214:171–179.

    Article  PubMed  CAS  Google Scholar 

  8. Parthasarathy S, Wieland E, and Steinberg D. 1989. A role for endothelial cell lipoxygenase in the oxidative modification of LDL. Proc Natl Acad Sci USA. 86:1046–1050.

    Article  PubMed  CAS  Google Scholar 

  9. Rankin SM, Parthasarathy S, and Steinberg D. 1991. Evidence for a dominant role of lipoxygenases in oxidation of LDL by mouse peritoneal macrophages. J Lipid Res. 32:449–456.

    PubMed  CAS  Google Scholar 

  10. Sigari F, Lee C, Witztum JL, and Reaven PD. 1997. Fibroblasts that overexpress 15-LO generate bioactive and minimally-modified LDL. Arterioscler. Thromb. Vasc Biol. 17: 3639–3645.

    Article  PubMed  CAS  Google Scholar 

  11. Sun D, and Funk CD. 1996. Disruption of 12/15 LO expression in peritoneal macrophages. J Biol Chem. 271:24055–24062.

    Article  PubMed  CAS  Google Scholar 

  12. Sparrow CP, and Olszewski J. 1992. Cellular oxidative modification of LDL does not require lipoxygenases. Proc Natl Acad Sci USA. 89:128–131.

    Article  PubMed  CAS  Google Scholar 

  13. Kim JA, Berliner JA, Natarajan RD, and Nadler JL. 1994. Evidence that glucose increases monocyte binding to human aortic endothelial cells. Diabetes. 43: 1103–1107.

    Article  PubMed  CAS  Google Scholar 

  14. Brown ML, Jakubowski JA, Leventis LL, and Deykin D. 1988. Elevated glucose alters eicosanoid release from porcine aortic endothelial cells. J Clin Invest. 82: 2136–2141.

    Article  PubMed  CAS  Google Scholar 

  15. Natarajan R, Gu J-L, Rossi J, Gonzales N, Lanting L, Xu L, and Nadler JL. 1993. Elevated glucose and angiotensin II increases12-lipoxygenase activity and expression in porcine aortic smooth muscle cells. Proc Natl Acad Sci USA. 90:4947–4951.

    Article  PubMed  CAS  Google Scholar 

  16. Berliner JA, Navab MN, Fogelman AM, Frank JS, Demer LL, Edwards PA, Watson AD, and Lusis AJ. 1995. Atherosclerosis: basic mechanisms. Oxidation, inflammation and genetics. Arterioscler. Thromb. Vasc. Biol. 91:2488–2496.

    CAS  Google Scholar 

  17. Kim JA, Gu J-L, Natarajan R, Berliner JA, and Nadler JL. 1995. A leukocyte type of 12-LO is expressed by human vascular and mononuclear cells: evidence for upregulation by angiotensin II. Arterioscler. Thromb. Vasc. Biol. 15: 942–948

    Article  PubMed  CAS  Google Scholar 

  18. Hynes RO. 1992. Integrins: versatility, modulation, and signaling in cell adhesion. Cell. 69:11–25.

    Article  PubMed  CAS  Google Scholar 

  19. Bevilacqua MP. 1993. Endothelial-leukocyte adhesion molecules. Annu Rev. Immunol. 11:767–804.

    Article  PubMed  CAS  Google Scholar 

  20. Butcher EC. 1991. Leukocyte:endothelial cell recognition: three (or more) steps to specificity and diversity. Cell. 67: 1033–1036.

    Article  PubMed  CAS  Google Scholar 

  21. McEver RP. 1992. Leukocyte-endothelial cell interactions. Current Opin Cell Biol. 4:840–849.

    Article  CAS  Google Scholar 

  22. Springer TA. 1990. Adhesion receptors of the immune system. Nature. 346:425–434.

    Article  PubMed  CAS  Google Scholar 

  23. Tang DG, Diglio CA, Bazaz R, and Honn KV. 1995. Transcriptional activation of endothelial cell integrin v by protein kinase C activator 12(S)-HETE. J Cell Sci. 108: 2629–2644.

    PubMed  CAS  Google Scholar 

  24. Trikha M and Honn KV. 1997. Role of 12-lipoxygenase and protein kinase C in modulating the activation state of the integrin aIIbB3 on human tumor cells. In: Eicosanoids and Other Bioactive Lipids in Cancer Inflammation and Radiation Injury 3. KV Honn, editor. Plenum Press, New York., 55–60.

    Google Scholar 

  25. Liu B, Khan WA, Hannun YA, Timar J, Taylor JD, Lundy S, Butovich I, and Honn KV. 1995. 12(S)-HETE and 13(S)-HODE regulation of protein kinase C in melanoma cells: role of receptor-mediated hydrolysis of inositol phospholipids. Proc Natl Acad Sci USA. 92: 9323–9327.

    Article  PubMed  CAS  Google Scholar 

  26. Muller WA, Weigl SA, Deng X, Phiilips DM. 1993. PECAM-1 is required for transendothelial migration of leukocytes. J Exp Med. 178:449–460.

    Article  PubMed  CAS  Google Scholar 

  27. Frenette PS, Johnson RC, Hynes RO, and Wagner DD. 1995. Platelets roll on stimulated endothelium in vivo: interaction mediated by endothelial p-selectin. Proc Natl Acad Sci USA. 92: 7450–7454.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1999 Springer Science+Business Media New York

About this chapter

Cite this chapter

Hedrick, C.C., Kim, M.D., Natarajan, R.D., Nadler, J.L. (1999). 12-Lipoxygenase Products Increase Monocyte: Endothelial Interactions. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E.A. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 4. Advances in Experimental Medicine and Biology, vol 469. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4793-8_67

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-4793-8_67

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7171-7

  • Online ISBN: 978-1-4615-4793-8

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics