Ablation of aryl hydrocarbon receptor promotes angiotensin II-induced cardiac fibrosis through enhanced c-Jun/HIF-1α signaling
Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been...
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| Published in | Archives of toxicology Vol. 93; no. 6; pp. 1543 - 1553 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.06.2019
Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (
Ahr
−/−
). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male
Ahr
−/−
and age-matched wild-type mice (
n
= 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in
Ahr
−/−
and wild-type mice. However,
Ahr
−/−
mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of
Ahr
−/−
mice, but not in wild-type mice, and significantly increased the c-Jun signaling in
Ahr
−/−
mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of
Ahr
−/−
mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. |
|---|---|
| AbstractList | Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (
Ahr
−/−
). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male
Ahr
−/−
and age-matched wild-type mice (
n
= 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in
Ahr
−/−
and wild-type mice. However,
Ahr
−/−
mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of
Ahr
−/−
mice, but not in wild-type mice, and significantly increased the c-Jun signaling in
Ahr
−/−
mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of
Ahr
−/−
mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (Ahr−/−). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male Ahr−/− and age-matched wild-type mice (n = 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in Ahr−/− and wild-type mice. However, Ahr−/− mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of Ahr−/− mice, but not in wild-type mice, and significantly increased the c-Jun signaling in Ahr−/− mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of Ahr−/− mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (Ahr ). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male Ahr and age-matched wild-type mice (n = 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in Ahr and wild-type mice. However, Ahr mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of Ahr mice, but not in wild-type mice, and significantly increased the c-Jun signaling in Ahr mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of Ahr mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene ( Ahr −/− ). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male Ahr −/− and age-matched wild-type mice ( n = 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in Ahr −/− and wild-type mice. However, Ahr −/− mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of Ahr −/− mice, but not in wild-type mice, and significantly increased the c-Jun signaling in Ahr −/− mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of Ahr −/− mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (Ahr-/-). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male Ahr-/- and age-matched wild-type mice (n = 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in Ahr-/- and wild-type mice. However, Ahr-/- mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of Ahr-/- mice, but not in wild-type mice, and significantly increased the c-Jun signaling in Ahr-/- mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of Ahr-/- mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling.Aryl hydrocarbon receptor (AHR) is a transcription factor that binds to DNA as a heterodimer with the AHR nuclear translocator (ARNT) after interaction with ligands, such as polycyclic and halogenated aromatic hydrocarbons and other xenobiotics. The endogenous ligands and functions of AHR have been the subject of many investigations. In the present study, the potential role of AHR signaling in the development of left ventricular hypertrophy and cardiac fibrosis by angiotensin II (Ang II) infusion was investigated in mice lacking the AHR gene (Ahr-/-). We also assessed the hypothesis that fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) activator, reduces cardiac fibrosis through the c-Jun signaling. Male Ahr-/- and age-matched wild-type mice (n = 8 per group) were infused with Ang II at 100 ng/kg/min daily for 2 weeks. Treatment with Ang II increased systolic blood pressure to comparable levels in Ahr-/- and wild-type mice. However, Ahr-/- mice developed severe cardiac fibrosis after Ang II infusion compared with wild-type mice. Ang II infusion also significantly increased the expression of endothelin in the left ventricles of Ahr-/- mice, but not in wild-type mice, and significantly increased the c-Jun signaling in Ahr-/- mice. Ang II infusion also significantly enhanced the expression of hypoxia-inducible factor-1α (HIF-1α) and the downstream target vascular endothelial growth factor (VEGF) in the left ventricles of Ahr-/- mice. These results suggested pathogenic roles for the AHR signaling pathway in the development of cardiac fibrosis. Treatment with fenofibrate reduced cardiac fibrosis and abrogated the effects of Ang II on the expression of endothelin, HIF-1α, and VEGF. The inhibitory effect of fenofibrate on cardiac fibrosis was mediated by suppression of VEGF expression through modulation of c-Jun/HIF-1α signaling. |
| Author | Gonzalez, Frank Suzuki, Yuka Ichihara, Sahoko Nakajima, Tamie Li, Ping Izuoka, Kiyora Ichihara, Gaku Mise, Nathan |
| AuthorAffiliation | 2 Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke 329-0498, Japan 4 Laboratory of Metabolism, Center of Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA 5 Present Address: Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China 6 Present Address: Department of Lifelong Sports and Health Sciences, Chubu University, Kasugai, Japan 3 Nagoya University Graduate School of Medicine, Nagoya, Japan 7 Present Address: Department of Occupational and Environmental Health, Tokyo University of Science, Noda, Japan 1 Graduate School of Regional Innovation Studies, Mie University, Tsu, Japan |
| AuthorAffiliation_xml | – name: 4 Laboratory of Metabolism, Center of Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD, USA – name: 5 Present Address: Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China – name: 1 Graduate School of Regional Innovation Studies, Mie University, Tsu, Japan – name: 3 Nagoya University Graduate School of Medicine, Nagoya, Japan – name: 7 Present Address: Department of Occupational and Environmental Health, Tokyo University of Science, Noda, Japan – name: 2 Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine, 3311-1 Yakushiji, Shimotsuke 329-0498, Japan – name: 6 Present Address: Department of Lifelong Sports and Health Sciences, Chubu University, Kasugai, Japan |
| Author_xml | – sequence: 1 givenname: Sahoko orcidid: 0000-0002-7224-0949 surname: Ichihara fullname: Ichihara, Sahoko email: saho@jichi.ac.jp organization: Graduate School of Regional Innovation Studies, Mie University, Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine – sequence: 2 givenname: Ping surname: Li fullname: Li, Ping organization: Nagoya University Graduate School of Medicine, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences, Peking Union Medical College – sequence: 3 givenname: Nathan surname: Mise fullname: Mise, Nathan organization: Department of Environmental and Preventive Medicine, Jichi Medical University School of Medicine – sequence: 4 givenname: Yuka surname: Suzuki fullname: Suzuki, Yuka organization: Graduate School of Regional Innovation Studies, Mie University – sequence: 5 givenname: Kiyora surname: Izuoka fullname: Izuoka, Kiyora organization: Graduate School of Regional Innovation Studies, Mie University – sequence: 6 givenname: Tamie surname: Nakajima fullname: Nakajima, Tamie organization: Nagoya University Graduate School of Medicine, Department of Lifelong Sports and Health Sciences, Chubu University – sequence: 7 givenname: Frank surname: Gonzalez fullname: Gonzalez, Frank organization: Laboratory of Metabolism, Center of Cancer Research, National Cancer Institute, National Institute of Health – sequence: 8 givenname: Gaku surname: Ichihara fullname: Ichihara, Gaku organization: Nagoya University Graduate School of Medicine, Department of Occupational and Environmental Health, Tokyo University of Science |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31016362$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Springer-Verlag GmbH Germany, part of Springer Nature 2019 Archives of Toxicology is a copyright of Springer, (2019). All Rights Reserved. |
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| Keywords | Fibrosis Cardiac hypertrophy HIF-1α AHR Angiotensin II PPARα Vascular endothelial growth factor |
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| SubjectTerms | Ablation AhR gene Angiotensin Angiotensin II Angiotensin II - toxicity Animals Aromatic compounds Aromatic hydrocarbons Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Biomedical and Life Sciences Biomedicine Blood pressure Blood Pressure - drug effects c-Jun protein Deoxyribonucleic acid DNA Endothelins Environmental Health Fenofibrate Fenofibrate - pharmacology Fibrosis Growth factors Halogenated hydrocarbons Heart Hydrocarbons Hypertrophy Hypertrophy, Left Ventricular - pathology Hypoxia Hypoxia-Inducible Factor 1, alpha Subunit - genetics Hypoxia-inducible factors JNK Mitogen-Activated Protein Kinases - genetics Ligands Male Mice Mice, Knockout Molecular Toxicology Myocardium - pathology Occupational Medicine/Industrial Medicine Pharmacology/Toxicology PPAR alpha - agonists Receptors, Aryl Hydrocarbon - genetics Receptors, Aryl Hydrocarbon - metabolism Rodents Signal transduction Signal Transduction - drug effects Signal Transduction - genetics Signaling Transcription factors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - biosynthesis Vascular Endothelial Growth Factor A - genetics Ventricle Xenobiotics |
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| Title | Ablation of aryl hydrocarbon receptor promotes angiotensin II-induced cardiac fibrosis through enhanced c-Jun/HIF-1α signaling |
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