Genome-Wide Association Study Identifies Novel Susceptibility Genes Associated with Coronary Artery Aneurysm Formation in Kawasaki Disease

Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as di...

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Published inPloS one Vol. 11; no. 5; p. e0154943
Main Authors Kuo, Ho-Chang, Li, Sung-Chou, Guo, Mindy Ming-Huey, Huang, Ying-Hsien, Yu, Hong-Ren, Huang, Fu-Chen, Jiao, Fuyong, Kuo, Hsing-Chun, Andrade, Jorge, Chan, Wen-Ching
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 12.05.2016
Public Library of Science (PLoS)
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Online AccessGet full text
ISSN1932-6203
1932-6203
DOI10.1371/journal.pone.0154943

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Abstract Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10(-9); OR = 32.22) and rs7922552 (P = 8.43 × 10(-9); OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10(-9); OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
AbstractList Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10 −9 ; OR = 32.22) and rs7922552 (P = 8.43 × 10 −9 ; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10 −9 ; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 10-9; OR = 32.22) and rs7922552 (P = 8.43 10-9; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 10-9; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 x 10.sup.-9 ; OR = 32.22) and rs7922552 (P = 8.43 x 10.sup.-9 ; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 x 10.sup.-9 ; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10−9; OR = 32.22) and rs7922552 (P = 8.43 × 10−9; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10−9; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20-25% of untreated with IVIG and 3-5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10(-9); OR = 32.22) and rs7922552 (P = 8.43 × 10(-9); OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10(-9); OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in childhood. Generally, 20–25% of untreated with IVIG and 3–5% of treated KD patients have been developed coronary artery lesions (CALs), such as dilatation and aneurysm. Understanding how coronary artery aneurysms (CAAs) are established and maintained in KD patients is therefore of great importance. Upon our previous genotyping data of 157 valid KD subjects, a genome-wide association study (GWAS) has been conducted among 11 (7%) CAA-developed KD patients to reveal five significant genetic variants passed pre-defined thresholds and resulted in two novel susceptibility protein-coding genes, which are NEBL (rs16921209 (P = 7.44 × 10 −9 ; OR = 32.22) and rs7922552 (P = 8.43 × 10 −9 ; OR = 32.0)) and TUBA3C (rs17076896 (P = 8.04 × 10 −9 ; OR = 21.03)). Their known functions have been reported to associate with cardiac muscle and tubulin, respectively. As a result, this might imply their putative roles of establishing CAAs during KD progression. Additionally, various model analyses have been utilized to determine dominant and recessive inheritance patterns of identified susceptibility mutations. Finally, all susceptibility genes hit by significant genetic variants were further investigated and the top three representative gene-ontology (GO) clusters were regulation of cell projection organization, neuron recognition, and peptidyl-threonine phosphorylation. Our results help to depict the potential routes of the pathogenesis of CAAs in KD patients and will facilitate researchers to improve the diagnosis and prognosis of KD in personalized medicine.
Audience Academic
Author Jiao, Fuyong
Kuo, Hsing-Chun
Andrade, Jorge
Kuo, Ho-Chang
Chan, Wen-Ching
Guo, Mindy Ming-Huey
Yu, Hong-Ren
Huang, Fu-Chen
Huang, Ying-Hsien
Li, Sung-Chou
AuthorAffiliation 1 Department of Pediatrics and Kawasaki Disease Center, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
2 Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
Weill Medical College of Cornell University, UNITED STATES
4 Department of Nursing, Chang Gung University of Science and Technology, Chiayi, Taiwan
5 Center for Research Informatics, The University of Chicago, Chicago, Illinois, 60637, United States of America
3 Children's Hospital of Shaanxi Provincial People's Hospital and Jiaotong University, Xi'an, China
AuthorAffiliation_xml – name: 4 Department of Nursing, Chang Gung University of Science and Technology, Chiayi, Taiwan
– name: 3 Children's Hospital of Shaanxi Provincial People's Hospital and Jiaotong University, Xi'an, China
– name: 5 Center for Research Informatics, The University of Chicago, Chicago, Illinois, 60637, United States of America
– name: Weill Medical College of Cornell University, UNITED STATES
– name: 1 Department of Pediatrics and Kawasaki Disease Center, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
– name: 2 Genomics and Proteomics Core Laboratory, Department of Medical Research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27171184$$D View this record in MEDLINE/PubMed
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– notice: 2016 Kuo et al 2016 Kuo et al
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Competing Interests: The authors have declared that no competing interests exist.
Conceived and designed the experiments: Ho-Chang Kuo WCC. Performed the experiments: Ho-Chang Kuo MMG YHH Hsing-Chun Kuo. Analyzed the data: WCC. Contributed reagents/materials/analysis tools: Ho-Chang Kuo MMG YHH HRY FCH FJ. Wrote the paper: WCC YHH JA Ho-Chang Kuo. Organised and collected data: SCL.
ORCID 0000-0003-0034-7277
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Snippet Kawasaki disease (KD) or Kawasaki syndrome is known as a vasculitis of small to medium-sized vessels, and coronary arteries are predominantly involved in...
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StartPage e0154943
SubjectTerms Aneurysm
Aneurysms
Arteries
Biology and Life Sciences
Blood vessels
Cardiac muscle
Cardiovascular disease
Child
Children
Coding
Coronary Aneurysm - complications
Coronary Aneurysm - genetics
Coronary arteries
Coronary artery
Coronary vessels
Coronary Vessels - pathology
Development and progression
DNA methylation
Drug dosages
Gene expression
Gene Ontology
Genes
Genetic aspects
Genetic diversity
Genetic Predisposition to Disease
Genetic variance
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genomics
Genotyping
Health risk assessment
Heart diseases
Heredity
Hospitals
Humans
Immunoglobulins
Informatics
Intravenous administration
Kawasaki disease
Kawasaki syndrome
Knowledge representation
Laboratories
Lesions
Linkage Disequilibrium - genetics
Matrix Metalloproteinase 9 - genetics
Medical research
Medicine
Medicine and Health Sciences
Models, Genetic
Mucocutaneous lymph node syndrome
Mucocutaneous Lymph Node Syndrome - complications
Mucocutaneous Lymph Node Syndrome - genetics
Muscles
Mutation
Neural coding
Pathogenesis
Patients
Pediatrics
Phosphorylation
Physiological aspects
Polymorphism, Single Nucleotide - genetics
Precision medicine
Proteomics
Risk Factors
Threonine
Tubulin
Tumor Necrosis Factor-alpha - genetics
Tumor necrosis factor-TNF
Vasculitis
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Title Genome-Wide Association Study Identifies Novel Susceptibility Genes Associated with Coronary Artery Aneurysm Formation in Kawasaki Disease
URI https://www.ncbi.nlm.nih.gov/pubmed/27171184
https://www.proquest.com/docview/1788543304
https://www.proquest.com/docview/1789495425
https://www.proquest.com/docview/1805501963
https://pubmed.ncbi.nlm.nih.gov/PMC4865092
https://doaj.org/article/e4db480cdc2f412997db93a4c22d0945
http://dx.doi.org/10.1371/journal.pone.0154943
Volume 11
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