Loss of heterozygosity of the NOS3 dinucleotide repeat marker in atherosclerotic plaques of human carotid arteries

Francesca R. Grati, Giorgio Ghilardi, Silvia M. Sirchia, Federico Massaro, Barbara Cassani, Roberto Scorza, Chiara De Andreis, Elena Sironi, Giuseppe Simoni

Research output: Contribution to journalArticle

Abstract

We have investigated 28 atherosclerotic plaques of human carotid arteries with a panel of 39 microsatellite markers for the presence of LOH. The objective of this research was to verify if LOH, described in association with tumorigenic process, could be involved also in benign fibroproliferative disease. Seventy percent of samples demonstrated allelic imbalance: 50% of cases showed LOH at a minimum of one locus, 3.5% at a minimum of two loci and 14.3% at three or more loci. The percentages of LOH ranged between 3.8 and 14.3% and the highest involved polymorphic marker is the NOS3 internal dinucleotide repeat. Our results indicate that, like tumorigenesis, the atherogenic process could also involve LOH mechanism. Furthermore, the finding regarding the NOS3 internal polymorphism suggests a possible role of the gene as cofactor in formation of the atheromas.

Original languageEnglish
Pages (from-to)261-267
Number of pages7
JournalAtherosclerosis
Volume159
Issue number2
DOIs
Publication statusPublished - 2001

Keywords

  • Atherosclerosis
  • Carotid
  • Hyperproliferation
  • LOH
  • NOS3
  • Plaque
  • Polymorphism

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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  • Cite this

    Grati, F. R., Ghilardi, G., Sirchia, S. M., Massaro, F., Cassani, B., Scorza, R., De Andreis, C., Sironi, E., & Simoni, G. (2001). Loss of heterozygosity of the NOS3 dinucleotide repeat marker in atherosclerotic plaques of human carotid arteries. Atherosclerosis, 159(2), 261-267. https://doi.org/10.1016/S0021-9150(01)00466-X