PUBLICATION

An APOO Pseudogene on Chromosome 5q is Associated with LDL-C Levels

Authors
Montasser, M.E., O'Hare, E.A., Wang, X., Howard, A.D., McFarland, R., Perry, J.A., Ryan, K.A., Rice, K., Jaquish, C.E., Shuldiner, A.R., Miller, M., Mitchell, B.D., Zaghloul, N.A., Chang, Y.C.
ID
ZDB-PUB-180330-2
Date
2018
Source
Circulation   138(13): 1343-1355 (Journal)
Registered Authors
McFarland, Rebecca, Zaghloul, Norann A.
Keywords
founder, gene mapping, genetics, low-density lipoprotein cholesterol, pseudogene
MeSH Terms
  • Amish/genetics*
  • Animals
  • Animals, Genetically Modified
  • Atherosclerosis/blood
  • Atherosclerosis/diagnosis
  • Atherosclerosis/ethnology
  • Atherosclerosis/genetics*
  • Cholesterol, LDL/blood*
  • Chromosomes, Human, Pair 5*
  • Dyslipidemias/blood
  • Dyslipidemias/diagnosis
  • Dyslipidemias/ethnology
  • Dyslipidemias/genetics*
  • Founder Effect
  • Genetic Association Studies
  • Genetic Predisposition to Disease
  • Haplotypes
  • Humans
  • Phenotype
  • Pseudogenes*
  • Recombination, Genetic
  • Risk Factors
  • Zebrafish/genetics
PubMed
29593015 Full text @ Circulation
Abstract
Background -Elevated levels of low-density lipoprotein cholesterol (LDL-C) are a major risk factor for CVD via its contribution to the development and progression of atherosclerotic lesions. While the genetic basis of LDL-C has been studied extensively, currently known genetic variants account for only ~20% of the variation in LDL-C levels.Methods-Through an array-based association analysis in 1,102 Amish subjects, we identified a variant strongly associated with LDL-C levels. Using a combination of genetic analyses, zebrafish models, and in in vitro experiments, we sought to identify the causal gene driving this association.Results-We identified a founder haplotype associated with a 15 mg/dL increase in LDL-C on chromosome 5. After recombination mapping, the associated region contained 8 candidate genes. Using a zebrafish model to evaluate the relevance of these genes to cholesterol metabolism, we found that expression of the transcribed pseudogene, APOOP1, increased LDL-C and vascular plaque formation.Conclusions-Based on these data, we propose that APOOP1regulates levels of LDL-C in humans, thus identifying a novel mechanism of lipid homeostasis.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping