TCF21 and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells
Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcriptio...
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| Published in | PLoS genetics Vol. 13; no. 5; p. e1006750 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
08.05.2017
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1553-7404 1553-7390 1553-7404 |
| DOI | 10.1371/journal.pgen.1006750 |
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| Abstract | Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcription factor TCF21 as the causal CAD gene at 6q23.2 and characterized its downstream transcriptional network that is enriched for CAD GWAS genes. Here we investigate the hypothesis that TCF21 interacts with a downstream target gene, the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor that mediates the cellular response to environmental contaminants, including dioxin and polycyclic aromatic hydrocarbons (e.g., tobacco smoke). Perturbation of TCF21 expression in human coronary artery smooth muscle cells (HCASMC) revealed that TCF21 promotes expression of AHR, its heterodimerization partner ARNT, and cooperates with these factors to upregulate a number of inflammatory downstream disease related genes including IL1A, MMP1, and CYP1A1. TCF21 was shown to bind in AHR, ARNT and downstream target gene loci, and co-localization was noted for AHR-ARNT and TCF21 binding sites genome-wide in regions of HCASMC open chromatin. These regions of co-localization were found to be enriched for GWAS signals associated with cardio-metabolic as well as chronic inflammatory disease phenotypes. Finally, we show that similar to TCF21, AHR gene expression is increased in atherosclerotic lesions in mice in vivo using laser capture microdissection, and AHR protein is localized in human carotid atherosclerotic lesions where it is associated with protein kinases with a critical role in innate immune response. These data suggest that TCF21 can cooperate with AHR to activate an inflammatory gene expression program that is exacerbated by environmental stimuli, and may contribute to the overall risk for CAD. |
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| AbstractList | Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcription factor TCF21 as the causal CAD gene at 6q23.2 and characterized its downstream transcriptional network that is enriched for CAD GWAS genes. Here we investigate the hypothesis that TCF21 interacts with a downstream target gene, the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor that mediates the cellular response to environmental contaminants, including dioxin and polycyclic aromatic hydrocarbons (e.g., tobacco smoke). Perturbation of TCF21 expression in human coronary artery smooth muscle cells (HCASMC) revealed that TCF21 promotes expression of AHR, its heterodimerization partner ARNT, and cooperates with these factors to upregulate a number of inflammatory downstream disease related genes including IL1A, MMP1, and CYP1A1. TCF21 was shown to bind in AHR, ARNT and downstream target gene loci, and co-localization was noted for AHR-ARNT and TCF21 binding sites genome-wide in regions of HCASMC open chromatin. These regions of co-localization were found to be enriched for GWAS signals associated with cardio-metabolic as well as chronic inflammatory disease phenotypes. Finally, we show that similar to TCF21, AHR gene expression is increased in atherosclerotic lesions in mice in vivo using laser capture microdissection, and AHR protein is localized in human carotid atherosclerotic lesions where it is associated with protein kinases with a critical role in innate immune response. These data suggest that TCF21 can cooperate with AHR to activate an inflammatory gene expression program that is exacerbated by environmental stimuli, and may contribute to the overall risk for CAD.Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcription factor TCF21 as the causal CAD gene at 6q23.2 and characterized its downstream transcriptional network that is enriched for CAD GWAS genes. Here we investigate the hypothesis that TCF21 interacts with a downstream target gene, the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor that mediates the cellular response to environmental contaminants, including dioxin and polycyclic aromatic hydrocarbons (e.g., tobacco smoke). Perturbation of TCF21 expression in human coronary artery smooth muscle cells (HCASMC) revealed that TCF21 promotes expression of AHR, its heterodimerization partner ARNT, and cooperates with these factors to upregulate a number of inflammatory downstream disease related genes including IL1A, MMP1, and CYP1A1. TCF21 was shown to bind in AHR, ARNT and downstream target gene loci, and co-localization was noted for AHR-ARNT and TCF21 binding sites genome-wide in regions of HCASMC open chromatin. These regions of co-localization were found to be enriched for GWAS signals associated with cardio-metabolic as well as chronic inflammatory disease phenotypes. Finally, we show that similar to TCF21, AHR gene expression is increased in atherosclerotic lesions in mice in vivo using laser capture microdissection, and AHR protein is localized in human carotid atherosclerotic lesions where it is associated with protein kinases with a critical role in innate immune response. These data suggest that TCF21 can cooperate with AHR to activate an inflammatory gene expression program that is exacerbated by environmental stimuli, and may contribute to the overall risk for CAD. Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcription factor TCF21 as the causal CAD gene at 6q23.2 and characterized its downstream transcriptional network that is enriched for CAD GWAS genes. Here we investigate the hypothesis that TCF21 interacts with a downstream target gene, the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor that mediates the cellular response to environmental contaminants, including dioxin and polycyclic aromatic hydrocarbons (e.g., tobacco smoke). Perturbation of TCF21 expression in human coronary artery smooth muscle cells (HCASMC) revealed that TCF21 promotes expression of AHR, its heterodimerization partner ARNT, and cooperates with these factors to upregulate a number of inflammatory downstream disease related genes including IL1A, MMP1, and CYP1A1. TCF21 was shown to bind in AHR, ARNT and downstream target gene loci, and co-localization was noted for AHR-ARNT and TCF21 binding sites genome-wide in regions of HCASMC open chromatin. These regions of co-localization were found to be enriched for GWAS signals associated with cardio-metabolic as well as chronic inflammatory disease phenotypes. Finally, we show that similar to TCF21, AHR gene expression is increased in atherosclerotic lesions in mice in vivo using laser capture microdissection, and AHR protein is localized in human carotid atherosclerotic lesions where it is associated with protein kinases with a critical role in innate immune response. These data suggest that TCF21 can cooperate with AHR to activate an inflammatory gene expression program that is exacerbated by environmental stimuli, and may contribute to the overall risk for CAD. Both environmental factors and genetic loci have been associated with coronary artery disease (CAD), however gene-gene and gene-environment interactions that might identify molecular mechanisms of risk are not easily studied by human genetic approaches. We have previously identified the transcription factor TCF21 as the causal CAD gene at 6q23.2 and characterized its downstream transcriptional network that is enriched for CAD GWAS genes. Here we investigate the hypothesis that TCF21 interacts with a downstream target gene, the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor that mediates the cellular response to environmental contaminants, including dioxin and polycyclic aromatic hydrocarbons (e.g., tobacco smoke). Perturbation of TCF21 expression in human coronary artery smooth muscle cells (HCASMC) revealed that TCF21 promotes expression of AHR , its heterodimerization partner ARNT , and cooperates with these factors to upregulate a number of inflammatory downstream disease related genes including IL1A , MMP1 , and CYP1A1 . TCF21 was shown to bind in AHR , ARNT and downstream target gene loci, and co-localization was noted for AHR-ARNT and TCF21 binding sites genome-wide in regions of HCASMC open chromatin. These regions of co-localization were found to be enriched for GWAS signals associated with cardio-metabolic as well as chronic inflammatory disease phenotypes. Finally, we show that similar to TCF21, AHR gene expression is increased in atherosclerotic lesions in mice in vivo using laser capture microdissection, and AHR protein is localized in human carotid atherosclerotic lesions where it is associated with protein kinases with a critical role in innate immune response. These data suggest that TCF21 can cooperate with AHR to activate an inflammatory gene expression program that is exacerbated by environmental stimuli, and may contribute to the overall risk for CAD. Coronary heart disease is the leading cause of death in the world. Both genes and the environment are important risk factors for the progression of disease, however, how genes may modulate the harmful response to the disease promoting environment is unknown and difficult to study. Here, we show that a common heritable variation in the gene TCF21 may regulate coronary heart disease risk by regulating the response of downstream gene activation by the disease environment. We find that a well-known environmental sensor, aryl-hydrocarbon receptor (AHR), is regulated by TCF21 and also interacts with TCF21, resulting in regulation of pro-inflammatory gene expression in coronary artery smooth muscle cells. We further show that oxidized LDL, a well-known driver of atherosclerosis in the plaque can activate the AHR pathway. This work describes a heritable form of gene-environment interaction identified through genome wide association studies in coronary artery disease, and presents an opportunity to define causal gene-gene and gene-environment interactions. |
| Audience | Academic |
| Author | Wang, Ting Nguyen, Trieu Liu, Boxiang Sazonova, Olga Pjanic, Milos Quertermous, Thomas Miller, Clint L. Iyer, Dharini Matic, Ljubica Perisic Hedin, Ulf Carcamo-Orive, Ivan Kim, Juyong Brian Maegdefessel, Lars |
| AuthorAffiliation | 2 Cardiovascular Institute, Stanford University, Stanford, California, United States of America Geisel School of Medicine at Dartmouth, UNITED STATES 1 Division of Cardiovascular Medicine, Stanford University, Stanford, California, United States of America 3 Department of Biology, Stanford University, Stanford, California, United States of America 4 Department of Molecular Medicine and Surgery, Karolinska Institute, Solna, Sweden |
| AuthorAffiliation_xml | – name: 4 Department of Molecular Medicine and Surgery, Karolinska Institute, Solna, Sweden – name: 1 Division of Cardiovascular Medicine, Stanford University, Stanford, California, United States of America – name: Geisel School of Medicine at Dartmouth, UNITED STATES – name: 2 Cardiovascular Institute, Stanford University, Stanford, California, United States of America – name: 3 Department of Biology, Stanford University, Stanford, California, United States of America |
| Author_xml | – sequence: 1 givenname: Juyong Brian orcidid: 0000-0002-9675-2607 surname: Kim fullname: Kim, Juyong Brian – sequence: 2 givenname: Milos orcidid: 0000-0001-9746-8838 surname: Pjanic fullname: Pjanic, Milos – sequence: 3 givenname: Trieu surname: Nguyen fullname: Nguyen, Trieu – sequence: 4 givenname: Clint L. orcidid: 0000-0003-4276-3607 surname: Miller fullname: Miller, Clint L. – sequence: 5 givenname: Dharini surname: Iyer fullname: Iyer, Dharini – sequence: 6 givenname: Boxiang surname: Liu fullname: Liu, Boxiang – sequence: 7 givenname: Ting surname: Wang fullname: Wang, Ting – sequence: 8 givenname: Olga surname: Sazonova fullname: Sazonova, Olga – sequence: 9 givenname: Ivan orcidid: 0000-0001-8823-4925 surname: Carcamo-Orive fullname: Carcamo-Orive, Ivan – sequence: 10 givenname: Ljubica Perisic surname: Matic fullname: Matic, Ljubica Perisic – sequence: 11 givenname: Lars surname: Maegdefessel fullname: Maegdefessel, Lars – sequence: 12 givenname: Ulf orcidid: 0000-0001-9212-3945 surname: Hedin fullname: Hedin, Ulf – sequence: 13 givenname: Thomas surname: Quertermous fullname: Quertermous, Thomas |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28481916$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:136007037$$DView record from Swedish Publication Index |
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| Copyright | COPYRIGHT 2017 Public Library of Science 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells. PLoS Genet 13(5): e1006750. https://doi.org/10.1371/journal.pgen.1006750 2017 Kim et al 2017 Kim et al 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells. PLoS Genet 13(5): e1006750. https://doi.org/10.1371/journal.pgen.1006750 |
| Copyright_xml | – notice: COPYRIGHT 2017 Public Library of Science – notice: 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells. PLoS Genet 13(5): e1006750. https://doi.org/10.1371/journal.pgen.1006750 – notice: 2017 Kim et al 2017 Kim et al – notice: 2017 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells. PLoS Genet 13(5): e1006750. https://doi.org/10.1371/journal.pgen.1006750 |
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| Notes | new_version ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceptualization: JBK MP TN OS TQ.Data curation: JBK MP OS.Formal analysis: JBK MP BL LPM.Funding acquisition: JBK TQ.Investigation: JBK MP BL LPM LM DI TW.Methodology: JBK MP CLM BL LPM UH.Project administration: JBK TQ.Resources: JBK TN ICO TQ.Software: MP BL.Supervision: TQ.Validation: JBK MP TQ.Visualization: JBK MP TQ.Writing – original draft: JBK MP TQ.Writing – review & editing: JBK MP CLM LPM LM UH TQ. The authors have declared that no competing interests exist. |
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| SubjectTerms | AhR gene Analysis Animals Arteriosclerosis Aryl Hydrocarbon Receptor Nuclear Translocator - genetics Aryl Hydrocarbon Receptor Nuclear Translocator - metabolism Atherosclerosis - genetics Atherosclerosis - metabolism Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Binding sites Biology Biology and Life Sciences Cad gene Cardiovascular disease Care and treatment Cells, Cultured Chromatin Chromosome 6 Contaminants Coronary artery Coronary artery disease Coronary heart disease Coronary vessels Coronary Vessels - cytology Coronary Vessels - metabolism Councils Cytochrome P-450 CYP1A1 - genetics Cytochrome P-450 CYP1A1 - metabolism Cytochrome P450 Dioxins Environmental effects Environmental factors Gene expression Genome-wide association studies Genomes Genomics Heart Heart diseases HEK293 Cells Humans Hydrocarbons Immune response Innate immunity Interleukin 1 Interleukin-1alpha - genetics Interleukin-1alpha - metabolism Kinases Lesions Localization Matrix Metalloproteinase 1 - genetics Matrix Metalloproteinase 1 - metabolism Medicine Medicine and Health Sciences Mice Mice, Inbred C57BL Molecular modelling Myocytes, Smooth Muscle - metabolism Polycyclic aromatic hydrocarbons Protein Binding Protein kinase Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Sensors Smoke Smooth muscle Surgery Tobacco Transcription factors |
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| Title | TCF21 and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells |
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