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6 results on '"Taka-aki Matsuyama"'

1. Atheroprotective Effects of Tumor Necrosis Factor–Stimulated Gene-6

Author

Rena Watanabe, MS, Hitomi Watanabe, MS, Yui Takahashi, BS, Miho Kojima, BS, Hanae Konii, BS, Kaho Watanabe, MS, Remina Shirai, MS, Kengo Sato, PhD, Taka-aki Matsuyama, MD, PhD, Hatsue Ishibashi-Ueda, MD, PhD, Yoshitaka Iso, MD, PhD, Shinji Koba, MD, PhD, Youichi Kobayashi, MD, PhD, Tsutomu Hirano, MD, PhD, and Takuya Watanabe, MD, PhD

Subjects
atherosclerosis, coronary artery disease, endothelial cell, macrophage, TSG-6, vascular smooth muscle cell, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Tumor necrosis factor–stimulated gene-6 (TSG-6), an anti-inflammatory protein, was shown to be localized in the neointima of injury-induced rat arteries. However, the modulatory effect of TSG-6 on atherogenesis has not yet been reported. We aimed to evaluate the atheroprotective effects of TSG-6 on human endothelial cells (HECs), human monocyte-derived macrophages (HMDMs), human aortic smooth muscle cells (HASMCs) in vitro, and aortic lesions in apolipoprotein E–deficient mice, along with expression levels of TSG-6 in coronary lesions and plasma from patients with coronary artery disease (CAD). TSG-6 was abundantly expressed in HECs, HMDMs, and HASMCs in vitro. TSG-6 significantly suppressed cell proliferation and lipopolysaccharide-induced up-regulation of monocyte chemotactic protein-1, intercellular adhesion molecule-1, and vascular adhesion molecule-1 in HECs. TSG-6 significantly suppressed inflammatory M1 phenotype and suppressed oxidized low-density lipoprotein–induced foam cell formation associated with down-regulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in HMDMs. In HASMCs, TSG-6 significantly suppressed migration and proliferation, but increased collagen-1 and -3 expressions. Four-week infusion of TSG-6 into apolipoprotein E–deficient mice significantly retarded the development of aortic atherosclerotic lesions with decreased vascular inflammation, monocyte/macrophage, and SMC contents and increased collagen fibers. In addition, it decreased peritoneal M1 macrophages with down-regulation of inflammatory molecules and lowered plasma total cholesterol levels. In patients with CAD, plasma TSG-6 levels were significantly increased, and TSG-6 was highly expressed in the fibrous cap within coronary atherosclerotic plaques. These results suggest that TSG-6 contributes to the prevention and stability of atherosclerotic plaques. Thus, TSG-6 may serve as a novel therapeutic target for CAD.

Published
2016
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2. Benefit of magnetic resonance–conditional cardiac resynchronization therapy defibrillator: A case of cardiac sarcoidosis–involved cervical extradural lesion

Author

Hiroshi Kawakami, MD, Takayuki Nagai, MD, PhD, Taka-aki Matsuyama, MD, PhD, Kazuhisa Nishimura, MD, PhD, Jitsuo Higaki, MD, PhD, and Akiyoshi Ogimoto, MD, PhD

Subjects
Cardiac resynchronization therapy defibrillator, Cardiac sarcoidosis, Corticosteroid treatment, Magnetic resonance–conditional device, Magnetic resonance imaging, Neurologic sarcoidosis, Diseases of the circulatory (Cardiovascular) system, RC666-701
Published
2016
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3. Pathology after combined epicardial and endocardial ablation for ventricular tachycardia in a postmortem heart with hypertrophic cardiomyopathy

Author

Kenzaburo Nakajima, MD, Koji Miyamoto, MD, PhD, Taka-aki Matsuyama, MD, PhD, Takashi Noda, MD, PhD, Hatsue Ishibashi-Ueda, MD, PhD, and Kengo Kusano, MD, PhD

Subjects
Hypertrophic cardiomyopathy, Pathology, Ablation, Ventricular tachycardia, Diseases of the circulatory (Cardiovascular) system, RC666-701
Published
2015
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4. Atheroprotective Effects of Tumor Necrosis Factor–Stimulated Gene-6

Author

Tsutomu Hirano, Kengo Sato, Hitomi Watanabe, Youichi Kobayashi, Taka aki Matsuyama, Yoshitaka Iso, Yui Takahashi, Kaho Watanabe, Shinji Koba, Takuya Watanabe, Remina Shirai, Hanae Konii, Hatsue Ishibashi-Ueda, Miho Kojima, and Rena Watanabe

Subjects
0301 basic medicine, Neointima, lcsh:Diseases of the circulatory (Cardiovascular) system, CD36, CAD, coronary artery disease, TSG, tumor necrosis factor stimulated gene, macrophage, 030204 cardiovascular system & hematology, ApoE−/−, apolipoprotein E deficient, VSMC, vascular smooth muscle cell, 03 medical and health sciences, PRECLINICAL RESEARCH, 0302 clinical medicine, HUVEC, human umbilical vein endothelial cell, medicine, Macrophage, TSG-6, Foam cell, HASMC, human aortic smooth muscle cell, biology, Chemistry, Monocyte, AngII, angiotensin II, Fibrous cap, ABCA1, ATP-binding cassette transporter A1, ECM, extracellular matrix, Endothelial stem cell, MMP, matrix metalloproteinase, 030104 developmental biology, medicine.anatomical_structure, HMDM, human monocyte-derived macrophage, oxLDL, oxidized low-density lipoprotein, lcsh:RC666-701, Immunology, Cancer research, biology.protein, endothelial cell, Tumor necrosis factor alpha, ACAT1, acyl-CoA:cholesterol acyltransferase-1, TIMP, tissue inhibitor of metalloproteinase, atherosclerosis, vascular smooth muscle cell, Cardiology and Cardiovascular Medicine, coronary artery disease
Abstract

Visual Abstract, Highlights • TSG-6 suppresses the development of atherosclerosis by decreasing inflammatory responses of endothelial cells and macrophages, endothelial proliferation, macrophage foam cell formation, and VSMC migration and proliferation. • TSG-6 also contributes to plaque stability by extracellular matrix production in the fibrous cap. • TSG-6 is expected to emerge as a new line of therapy against atherosclerosis and CAD. • This study also provides insights into the potential use of TSG-6 as a biomarker for CAD. • These findings may strengthen the clinical utility of TSG-6 in the diagnosis and treatment of CAD., Summary Tumor necrosis factor–stimulated gene-6 (TSG-6), an anti-inflammatory protein, was shown to be localized in the neointima of injury-induced rat arteries. However, the modulatory effect of TSG-6 on atherogenesis has not yet been reported. We aimed to evaluate the atheroprotective effects of TSG-6 on human endothelial cells (HECs), human monocyte-derived macrophages (HMDMs), human aortic smooth muscle cells (HASMCs) in vitro, and aortic lesions in apolipoprotein E–deficient mice, along with expression levels of TSG-6 in coronary lesions and plasma from patients with coronary artery disease (CAD). TSG-6 was abundantly expressed in HECs, HMDMs, and HASMCs in vitro. TSG-6 significantly suppressed cell proliferation and lipopolysaccharide-induced up-regulation of monocyte chemotactic protein-1, intercellular adhesion molecule-1, and vascular adhesion molecule-1 in HECs. TSG-6 significantly suppressed inflammatory M1 phenotype and suppressed oxidized low-density lipoprotein–induced foam cell formation associated with down-regulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in HMDMs. In HASMCs, TSG-6 significantly suppressed migration and proliferation, but increased collagen-1 and -3 expressions. Four-week infusion of TSG-6 into apolipoprotein E–deficient mice significantly retarded the development of aortic atherosclerotic lesions with decreased vascular inflammation, monocyte/macrophage, and SMC contents and increased collagen fibers. In addition, it decreased peritoneal M1 macrophages with down-regulation of inflammatory molecules and lowered plasma total cholesterol levels. In patients with CAD, plasma TSG-6 levels were significantly increased, and TSG-6 was highly expressed in the fibrous cap within coronary atherosclerotic plaques. These results suggest that TSG-6 contributes to the prevention and stability of atherosclerotic plaques. Thus, TSG-6 may serve as a novel therapeutic target for CAD.

Published
2016

5. Benefit of magnetic resonance–conditional cardiac resynchronization therapy defibrillator: A case of cardiac sarcoidosis–involved cervical extradural lesion

Author

Jitsuo Higaki, Hiroshi Kawakami, Akiyoshi Ogimoto, Kazuhisa Nishimura, Takayuki Nagai, and Taka-aki Matsuyama

Subjects
Corticosteroid treatment, medicine.medical_specialty, lcsh:Diseases of the circulatory (Cardiovascular) system, Neurologic sarcoidosis, medicine.medical_treatment, Cardiac resynchronization therapy, Case Report, Cardiac sarcoidosis, 030204 cardiovascular system & hematology, Ventricular tachycardia, MR, magnetic resonance, LVEF - Left ventricular ejection fraction, Lesion, 03 medical and health sciences, 0302 clinical medicine, 18F-FDG, fluorine-18-fluorodeoxyglucose, Magnetic resonance imaging, Cardiac resynchronization therapy defibrillator, Internal medicine, LVEF, left ventricular ejection fraction, medicine, VT, ventricular tachycardia, Diseases of the circulatory (Cardiovascular) system, Ejection fraction, medicine.diagnostic_test, business.industry, medicine.disease, Implantable cardioverter-defibrillator, ICD, implantable cardioverter-defibrillator, Magnetic resonance–conditional device, CRT-D, cardiac resynchronization therapy defibrillator, lcsh:RC666-701, RC666-701, Cardiology, Radiology, medicine.symptom, Cardiology and Cardiovascular Medicine, business, MRI, magnetic resonance imaging, 030217 neurology & neurosurgery
Published
2016

6. Pathology after combined epicardial and endocardial ablation for ventricular tachycardia in a postmortem heart with hypertrophic cardiomyopathy

Author

Taka-aki Matsuyama, Takashi Noda, Hatsue Ishibashi-Ueda, Kengo Kusano, Koji Miyamoto, and Kenzaburo Nakajima

Subjects
medicine.medical_specialty, Pathology, HCM, hypertrophic cardiomyopathy, medicine.medical_treatment, Case Report, HCM - Hypertrophic cardiomyopathy, Ablation, Ventricular tachycardia, Internal medicine, medicine, VT, ventricular tachycardia, Diseases of the circulatory (Cardiovascular) system, RF, radiofrequency, LVZ, low-voltage zone, business.industry, RFCA, radiofrequency catheter ablation, Hypertrophic cardiomyopathy, medicine.disease, NICM, nonischemic cardiomyopathy, Nonischemic cardiomyopathy, LV, left ventricle, Radiofrequency catheter ablation, RC666-701, Cardiology, ECG, electrocardiogram, VT - Ventricular tachycardia, Cardiology and Cardiovascular Medicine, business
Published
2015

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