RGD Reference Report - Neointimal hyperplasia and vasoreactivity are controlled by genetic elements on rat chromosome 3. - Rat Genome Database

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Neointimal hyperplasia and vasoreactivity are controlled by genetic elements on rat chromosome 3.

Authors: Nestor Kalinoski, AL  Ramdath, RS  Langenderfer, KM  Sikanderkhel, S  Deraedt, S  Welch, M  Park, JL  Pringle, T  Joe, B  Cicila, GT  Allison, DC 
Citation: Nestor Kalinoski AL, etal., Hypertension. 2010 Feb;55(2):555-61. Epub 2009 Dec 21.
RGD ID: 2316923
Pubmed: PMID:20026763   (View Abstract at PubMed)
PMCID: PMC3765071   (View Article at PubMed Central)
DOI: DOI:10.1161/HYPERTENSIONAHA.109.142505   (Journal Full-text)

Neointimal hyperplasia (NIH) can lead to restenosis after clinical vascular interventions. NIH results from complex and poorly understood interactions between signaling cascades in the extracellular matrix and the disrupted endothelium, which lead to vessel occlusion. Quantitative trait loci (QTLs) were reported previously on rat chromosomes 3 and 6 through linkage analysis of postinjury NIH in midiliac arterial sections. In the current study, substitution mapping validated the RNO3 NIH QTL but not the RNO6 NIH QTL. The SHR.BN3 congenic strain had a 3-fold increase in the percentage of NIH compared with the parental spontaneously hypertensive rat strain. A double congenic study of RNO3+RNO6 NIH QTL segments suggested less than additive effects of these 2 genomic regions. To test the hypothesis that changes in vessel dynamics account for the differences in NIH formation, we performed vascular reactivity studies in the Brown Norway (BN), spontaneously hypertensive rat (SHR), SHR.BN3, and SHR.BN6 strains. De-endothelialized left common carotid artery rings of the SHR.BN3 showed an increased vascular responsiveness when treated with serotonin or prostaglandin F2(alpha), with significant differences in EC(50) and maximum effect (P<0.01) values compared with the spontaneously hypertensive rat parental strain. Because both vascular reactivity and percentage of NIH formation in the SHR.BN3 strain are significantly higher than the SHR strain, we postulate that these traits may be associated and are controlled by genetic elements on RNO3. In summary, these results confirm that the RNO3 NIH QTL carries the gene(s) contributing to postinjury NIH formation.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SHR.BN-(D3Rat159-D3Rat1)(D6Rat40-D6Rat170)/McoRatHyperplasia  IAGP  RGD 
SHR.BN-(D3Rat159-D3Rat1)/McoRatHyperplasia  IAGP  RGD 
SHR.BN-(D6Rat40-D6Rat170)/McoRatHyperplasia  IAGP  RGD 
SHR/NHsdRatHyperplasia susceptibilityIAGP  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Objects Annotated

Vnigr3  (Vascular neointimal growth QTL 3)

Additional Information