Skip to main content
The Journal of Experimental Medicine logoLink to The Journal of Experimental Medicine
. 1986 Oct 1;164(4):1171–1178. doi: 10.1084/jem.164.4.1171

Aging and arteriosclerosis. I. Development of myointimal hyperplasia after endothelial injury

PMCID: PMC2188432  PMID: 3760777

Abstract

Old Fischer 344 rats are more susceptible to vascular lesions after arterial endothelial injury than are young animals. Thus, 20-26-mo-old Fischer 344 rats developed greater and more persistent intimal proliferative lesions than did 2-5-mo-old rats after aortic endothelial denudation. 3 d after deendothelialization, intimal thickness was increased two-fold in both old and young animals. However, 14 d after endothelial injury, intimal thickness had increased nearly five times in old animals, but had regressed to normal in young animals. Intimal thickness of young aortic grafts transplanted into young recipients did not differ significantly from adjacent host aorta or autotransplanted aortic segments 6 wk after surgery. In contrast, intimal thickness of old grafts transplanted into young recipients was eight times greater than adjacent young host aorta 6 wk after surgery. The density of cell nuclei in the intima of old grafts was also much greater than that in young grafts. Thus, in two experimental models of vascular injury, old rats have consistently had greater myointimal hyperplasia than young rats. The increased proliferative response of aortic smooth muscle cells after vascular injury of old animals may contribute to the increased prevalence of vascular disease with age.

Full Text

The Full Text of this article is available as a PDF (567.4 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. BAUMGARTNER H. R. EINE NEUE METHODE ZUR ERZEUGUNG VON THROMBEN DURCH GEZIELTE UBERDEHNUNG DER GEFAESSWAND. Z Gesamte Exp Med. 1963 Sep 12;137:227–247. [PubMed] [Google Scholar]
  2. Callard R. E., Basten A., Blanden R. V. Loss of immune competence with age may be due to a qualitative abnormality in lymphocyte membranes. Nature. 1979 Sep 20;281(5728):218–220. doi: 10.1038/281218a0. [DOI] [PubMed] [Google Scholar]
  3. Gozes Y., Umiel T., Meshorer A., Trainin N. Syngeneic GvH induced in popliteal lymph nodes by spleen cells of old C57BL/6 mice. J Immunol. 1978 Dec;121(6):2199–2204. [PubMed] [Google Scholar]
  4. Ross R., Glomset J. A. Atherosclerosis and the arterial smooth muscle cell: Proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Science. 1973 Jun 29;180(4093):1332–1339. doi: 10.1126/science.180.4093.1332. [DOI] [PubMed] [Google Scholar]
  5. Ross R., Glomset J., Harker L. Response to injury and atherogenesis. Am J Pathol. 1977 Mar;86(3):675–684. [PMC free article] [PubMed] [Google Scholar]
  6. Ross R. The pathogenesis of atherosclerosis--an update. N Engl J Med. 1986 Feb 20;314(8):488–500. doi: 10.1056/NEJM198602203140806. [DOI] [PubMed] [Google Scholar]
  7. Ross R., Wight T. N., Strandness E., Thiele B. Human atherosclerosis. I. Cell constitution and characteristics of advanced lesions of the superficial femoral artery. Am J Pathol. 1984 Jan;114(1):79–93. [PMC free article] [PubMed] [Google Scholar]
  8. Stemerman M. B., Weinstein R., Rowe J. W., Maciag T., Fuhro R., Gardner R. Vascular smooth muscle cell growth kinetics in vivo in aged rats. Proc Natl Acad Sci U S A. 1982 Jun;79(12):3863–3866. doi: 10.1073/pnas.79.12.3863. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from The Journal of Experimental Medicine are provided here courtesy of The Rockefeller University Press

RESOURCES