RGD Reference Report - Genetic analysis for a shared biological basis between migraine and coronary artery disease. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

Genetic analysis for a shared biological basis between migraine and coronary artery disease.

Authors: Winsvold, Bendik S  Nelson, Christopher P  Malik, Rainer  Gormley, Padhraig  Anttila, Verneri  Vander Heiden, Jason  Elliott, Katherine S  Jacobsen, Line M  Palta, Priit  Amin, Najaf  de Vries, Boukje  Hämäläinen, Eija  Freilinger, Tobias  Ikram, M Arfan  Kessler, Thorsten  Koiranen, Markku  Ligthart, Lannie  McMahon, George  Pedersen, Linda M  Willenborg, Christina  Won, Hong-Hee  Olesen, Jes  Artto, Ville  Assimes, Themistocles L  Blankenberg, Stefan  Boomsma, Dorret I  Cherkas, Lynn  Davey Smith, George  Epstein, Stephen E  Erdmann, Jeanette  Ferrari, Michel D  Göbel, Hartmut  Hall, Alistair S  Jarvelin, Marjo-Riitta  Kallela, Mikko  Kaprio, Jaakko  Kathiresan, Sekar  Lehtimäki, Terho  McPherson, Ruth  März, Winfried  Nyholt, Dale R  O'Donnell, Christopher J  Quaye, Lydia  Rader, Daniel J  Raitakari, Olli  Roberts, Robert  Schunkert, Heribert  Schürks, Markus  Stewart, Alexandre F R  Terwindt, Gisela M  Thorsteinsdottir, Unnur  van den Maagdenberg, Arn M J M  van Duijn, Cornelia  Wessman, Maija  Kurth, Tobias  Kubisch, Christian  Dichgans, Martin  Chasman, Daniel I  Cotsapas, Chris  Zwart, John-Anker  Samani, Nilesh J  Palotie, Aarno  CARDIoGRAM Consortium and the International Headache Genetics Consortium,  
Citation: Winsvold BS, etal., Neurol Genet. 2015 Jul 2;1(1):e10. doi: 10.1212/NXG.0000000000000010. eCollection 2015 Jun.
RGD ID: 401901243
Pubmed: PMID:27066539   (View Abstract at PubMed)
PMCID: PMC4821079   (View Article at PubMed Central)
DOI: DOI:10.1212/NXG.0000000000000010   (Journal Full-text)


OBJECTIVE: To apply genetic analysis of genome-wide association data to study the extent and nature of a shared biological basis between migraine and coronary artery disease (CAD).
METHODS: Four separate methods for cross-phenotype genetic analysis were applied on data from 2 large-scale genome-wide association studies of migraine (19,981 cases, 56,667 controls) and CAD (21,076 cases, 63,014 controls). The first 2 methods quantified the extent of overlapping risk variants and assessed the load of CAD risk loci in migraineurs. Genomic regions of shared risk were then identified by analysis of covariance patterns between the 2 phenotypes and by querying known genome-wide significant loci.
RESULTS: We found a significant overlap of genetic risk loci for migraine and CAD. When stratified by migraine subtype, this was limited to migraine without aura, and the overlap was protective in that patients with migraine had a lower load of CAD risk alleles than controls. Genes indicated by 16 shared risk loci point to mechanisms with potential roles in migraine pathogenesis and CAD, including endothelial dysfunction (PHACTR1) and insulin homeostasis (GIP).
CONCLUSIONS: The results suggest that shared biological processes contribute to risk of migraine and CAD, but surprisingly this commonality is restricted to migraine without aura and the impact is in opposite directions. Understanding the mechanisms underlying these processes and their opposite relationship to migraine and CAD may improve our understanding of both disorders.



RGD Manual Disease Annotations    Click to see Annotation Detail View
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
PHACTR1Humancoronary artery disease susceptibilityIAGP DNA:SNP:exon: (rs4714955) (human)RGD 
Phactr1Ratcoronary artery disease susceptibilityISOPHACTR1 (Homo sapiens)DNA:SNP:exon: (rs4714955) (human)RGD 
Phactr1Mousecoronary artery disease susceptibilityISOPHACTR1 (Homo sapiens)DNA:SNP:exon: (rs4714955) (human)RGD 
PHACTR1Humanmigraine  IAGP DNA:SNP:intron:g.13011943 (rs9349379) (human)RGD 
Phactr1Ratmigraine  ISOPHACTR1 (Homo sapiens)DNA:SNP:intron:g.13011943 (rs9349379) (human)RGD 
Phactr1Mousemigraine  ISOPHACTR1 (Homo sapiens)DNA:SNP:intron:g.13011943 (rs9349379) (human)RGD 

Phenotype Annotations    Click to see Annotation Detail View

Manual Human Phenotype Annotations - RGD

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
PHACTR1HumanCoronary artery atherosclerosis susceptibilityIAGP DNA:SNP:exon: (rs4714955)RGD 
PHACTR1HumanMigraine  IAGP DNA:SNP:intron:g.13011943 (rs9349379)RGD 
Objects Annotated

Genes (Rattus norvegicus)
Phactr1  (phosphatase and actin regulator 1)

Genes (Mus musculus)
Phactr1  (phosphatase and actin regulator 1)

Genes (Homo sapiens)
PHACTR1  (phosphatase and actin regulator 1)


Additional Information