RGD Reference Report - Linkage Analysis of Neointimal Hyperplasia and Vascular Wall Transformation Following Balloon Angioplasty. - Rat Genome Database

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Linkage Analysis of Neointimal Hyperplasia and Vascular Wall Transformation Following Balloon Angioplasty.

Authors: Nestor, AL  Cicila, GT  Karol, SE  Langenderfer, KM  Hollopeter, SL  Allison, DC 
Citation: Nestor AL, etal., Physiol Genomics. 2006 Jan 24;.
RGD ID: 1578306
Pubmed: PMID:16434542   (View Abstract at PubMed)
DOI: DOI:10.1152/physiolgenomics.00135.2005   (Journal Full-text)

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 utilized a rat model to find the genetic regions controlling NIH after endothelial denudation in two divergent inbred strains of rats. The BN and SHR rat 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 eight weeks post-injury to identify quantitative trait loci (QTL) responsible for this strain difference. Interval mapping identified two %NIH QTL on rat chromosomes 3 and 6 (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 linkage exists between these control-vessel parameters and NIH production. These results represent the first genetic analysis for the identification of neointimal hyperplasia QTL and QTL associated with the vascular injury response.




Disease Annotations    
Hyperplasia  (IAGP)


Objects Annotated

QTLs
Vnigr1  (Vascular neointimal growth QTL 1)
Vnigr2  (Vascular neointimal growth QTL 2)
Vnigr3  (Vascular neointimal growth QTL 3)

Strains
BN/SsNHsd  (NA)
SHR/NHsd  (NA)


Additional Information