RGD Reference Report - Identification of quantitative trait loci for serum cholesterol levels in stroke-prone spontaneously hypertensive rats. - Rat Genome Database

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Identification of quantitative trait loci for serum cholesterol levels in stroke-prone spontaneously hypertensive rats.

Authors: Kato, N  Amada T, T  Nabika, T  Ueno, K  Gotoda, T  Matsumoto, C  Mashimo, T  Sawamura, M  Ikeda, K  Nara, Y  Amori Y, Y 
Citation: Kato N, etal., Arterioscler Thromb Vasc Biol 2000 Jan;20(1):223-9
RGD ID: 61092
Web Url: http://www.atvbaha.org/cgi/content/abstract/20/1/223
Pubmed: PMID:10634822   (View Abstract at PubMed)

The stroke-prone spontaneously hypertensive rat (SHRSP) has been reported to show significantly lower levels of serum total cholesterol than the normotensive control strain Wistar-Kyoto rat (WKY). Because selective inbreeding was conducted for stroke proneness, this concomitantly inherited characteristic of SHRSP may play some pathophysiological role in stroke. We evaluated the genetic determinants of the cholesterol trait by estimating heritability and subsequently by undertaking a genome-wide screen with 161 genetic markers in F(2) progeny involving SHRSP and WKY (104 male and 106 female rats). Three quantitative trait loci (QTLs) were detected on rat chromosomes 5, 7, and 15. Markers from the linked region on chromosome 15 indicated significant evidence of linkage with a maximal log of the odds (LOD) score of 7.7, whereas those on chromosomes 5 and 7 cosegregated with the trait in a sex-specific manner (the QTL close to genetic marker D5 Mit5 reached an LOD score of 7.3 in males, and that close to D7 Mit10 reached an LOD score of 3.2 in females). The male-specific QTL on chromosome 5 appeared to overlap with previously reported QTLs for stroke-associated phenotypes, but an identical gene (or genes) appeared unlikely to control these and the cholesterol traits simultaneously. In the present study, serum cholesterol levels were shown to be highly genetically determined in SHRSP (the heritability estimates are 76% in males and 83% in females), and 3 QTLs with substantial effects were identified. Further work, however, is required to clarify whether the cholesterol trait is related to the etiology of stroke or has been retained by chance through the inbreeding process in SHRSP.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Scl1RatHypercholesterolemia  IDA  RGD 
Scl2RatHypercholesterolemia  IDA  RGD 
Scl3RatHypercholesterolemia  IDA  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Scl1Ratdecreased circulating cholesterol level  QTM  RGD 
Scl2Ratdecreased circulating cholesterol level  QTM  RGD 
Scl3Ratdecreased circulating cholesterol level  QTM  RGD 
SHRSP/A3Ratincreased circulating cholesterol level sexual_dimorphismIAGP compared to male SHRSP/A3RGD 
WKY/IzmRatincreased circulating cholesterol level sexual_dimorphismIAGP compared to male WKY/IzmRGD 

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Rat Strains:
Clinical Measurements:
Experimental Conditions:
Measurement Methods:
Objects Annotated

QTLs
Scl1  (Serum cholesterol level QTL 1)
Scl2  (Serum cholesterol level QTL 2)
Scl3  (Serum cholesterol level QTL 3)

Strains
SHRSP/A3  (NA)
WKY/Izm  (Wistar-Kyoto)

Objects referenced in this article
Marker D7Mit10 D7Mit10 Rattus norvegicus
Marker D5Mit5 D5Mit5 Rattus norvegicus
Marker D15Mgh2 D15Mgh2 Rattus norvegicus

Additional Information