Injury produces early rise in lipoprotein lipase activity in rabbit aorta

José Pablo Werba, Luis Alberto Cuniberti, Rubén Pedro Laguens, Lucas Daniel Masnatta, Ricardo Horacio Rey, Roberto Levy, Ricardo Horacio Pichel

Research output: Contribution to journalArticle

Abstract

The mechanisms following intimal injury predisposing towards atherosclerotic changes have not been fully elucidated. We speculated that a local increase in the enzyme lipoprotein lipase (LPL) might explain a higher susceptibility of the damaged intima to lipid accretion, and so we investigated the effect of balloon endothelial denudation on LPL activity and cholesterol content (LPL(a) and Chol(c), respectively), in aortas from normolipidemic male New Zealand white rabbits. Arteries were obtained from injured and control animals after 2, 6, 8 and 10 weeks to evaluate the shortest period after de-endothelialization necessary to detect LPL(a) changes. Injury resulted in a 4-fold LPL(a) rise (P <0.01), as early as 2 weeks, and the enzymatic activity remained increased throughout the study period. A mild but significant 22% Chol(c) increase (P <0.03) was found after 2 weeks of injury, even in this normolipidemic rabbit model. We conclude that physical damage to the intima markedly and soon increases LPL(a). This finding might account for the higher lipid accumulation by injured vessels, providing additional support to the hypothesis of LPL as an atherogenic mediator.

Original languageEnglish
Pages (from-to)257-266
Number of pages10
JournalAtherosclerosis
Volume125
Issue number2
DOIs
Publication statusPublished - Sep 6 1996

Keywords

  • Animal model
  • Atherosclerosis
  • Intimal proliferation
  • Lipoprotein lipase

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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  • Cite this

    Werba, J. P., Cuniberti, L. A., Laguens, R. P., Masnatta, L. D., Rey, R. H., Levy, R., & Pichel, R. H. (1996). Injury produces early rise in lipoprotein lipase activity in rabbit aorta. Atherosclerosis, 125(2), 257-266. https://doi.org/10.1016/0021-9150(96)05886-8