Linkage analysis of neointimal hyperplasia and vascular wall transformation after balloon angioplasty

Andrea L. Nestor, George T. Cicila, Seth E. Karol, Kay M. Langenderfer, Stacy L. Hollopeter, David C. Allison

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Neointimal hyperplasia (NIH), a result of vascular injury, is due to the migration and proliferation of smooth muscle cells through the media and internal elastic lamina leading to vascular occlusion. We used a rat model to find the genetic regions controlling NIH after endothelial denudation in two divergent inbred strains of rats. The Brown Norway (BN) and spontaneously hypertensive rat (SHR) strains have a 2.5-fold difference in injury-induced NIH. A population of 301 F2 (SHR X BN) rats underwent a standard vascular injury followed by phenotyping 8 wk after injury to identify quantitative trait loci (QTL) responsible for this strain difference. Interval mapping identified two %NIH QTL on rat chromosomes 3 and 6 [logarithm of odds (LOD) scores 2.5, 2.2] and QTL for other injured vascular wall changes on rat chromosomes 3, 4, and 15 (LOD scores 2.0-4.6). Also, QTL for control vessel media width (MW) and media area (MA) were found on chromosome 6 with LOD scores of 2.3 and 2.5, suggesting that linkage exists between these control vessel parameters and NIH production. These results represent the first genetic analysis for the identification of NIH QTL and QTL associated with the vascular injury response.

Original languageEnglish (US)
Pages (from-to)286-293
Number of pages8
JournalPhysiological Genomics
Issue number2
StatePublished - Apr 13 2006


  • Brown Norway rat
  • Inbred strains
  • Quantitative trait loci
  • Restenosis
  • Spontaneously hypertensive rat
  • Vascular injury

ASJC Scopus subject areas

  • Physiology
  • Genetics


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