Chisato Takamura
Tokyo Medical and Dental University
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Publication
Featured researches published by Chisato Takamura.
Journal of Cardiology | 2017
Natsuko Tamura; Yasuhiro Maejima; Daisuke Tezuka; Chisato Takamura; Shunji Yoshikawa; Takashi Ashikaga; Kenzo Hirao; Mitsuaki Isobe
BACKGROUND Takayasu arteritis (TA) is an autoimmune arteritis of unknown etiology. Currently, the erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP) levels are widely used to monitor disease activity of TA. However, sometimes it is difficult to reflect inflammatory symptoms in either CRP or ESR values, especially in TA patients with immunosuppressive therapies. Therefore, higher-accuracy biomarkers for evaluating disease activity need to be explored. METHODS AND RESULTS We examined 21 Japanese patients diagnosed with TA; 17 TA patients were treated with prednisone with or without additional immunosuppressive therapies and the remaining 4 patients were treated with infliximab, a human monoclonal anti-tumor necrosis factor (TNF)-α antibody. In active phase, the serum levels of both TNF-α and interleukin (IL)-6 were significantly higher than in healthy subjects, as is the case with both the levels of CRP and ESR. In contrast, the levels of both IL-12 and IL-23 remained in the normal range. Both TNF-α and IL-6 levels were markedly decreased in response to therapies, on equality with both CRP and ESR levels. Regarding the TA patients treated with infliximab, both CRP and IL-6 levels tended to be decreased after infliximab therapy. Conversely, TNF-α level after infliximab therapy was higher than before therapy. CONCLUSION Both TNF-α and IL-6 levels, but not IL-12 or IL-23 levels, in the serum could be potent biomarkers that can reflect the activity of TA.
American Journal of Physiology-heart and Circulatory Physiology | 2013
Norihiko Ashigaki; Jun-ichi Suzuki; Masahito Ogawa; Ryo Watanabe; Norio Aoyama; Naho Kobayashi; Tomoya Hanatani; Asuka Sekinishi; Hirofumi Zempo; Yuko Tada; Chisato Takamura; Kouji Wakayama; Yasunobu Hirata; Ryozo Nagai; Yuichi Izumi; Mitsuaki Isobe
Periodontitis is one of the most common infections in humans. Recently, published reports assert that periodontitis is associated with cardiovascular disease. Although it is said that viral, bacterial infections and autoimmune diseases may be the cause of myocarditis, the pathogenesis of it remains unclear. The aim of this study was to investigate the influence of a periodontal pathogen on experimental autoimmune myocarditis (EAM). Porphyromonas gingivalis (P.g.), PBS as a control, were injected into the mice. Histopathological and immunohistochemical analyses were performed. We examined heart mRNA levels using quantitative RT-PCR. The anti-P.g. IgG antibody level in plasma samples of the P.g.-injected group significantly increased compared with the PBS-injected group. Histopathological analysis detected that the myocarditis-affected areas and the fibrotic area in the P.g.-injected EAM group significantly increased compared with the PBS-injected EAM group (P < 0.05). Immunohistochemical analysis detected that more CD11b-positive cells were shown in the heart of the P.g.-injected EAM group compared with the PBS EAM-injected group (P < 0.05). Hearts from the P.g.-injected EAM group showed significantly increased expression of monocyte chemoattractant protein-1, IFN-γ, and matrix metalloproteinase-9 (MMP-9) mRNA compared with the hearts from the PBS-injected EAM group (P < 0.05). On day 7, serum levels of IL-6 were significantly enhanced in the P.g.-injected EAM group compared with the PBS-injected EAM group (P < 0.05). These results showed that P.g. injection could deteriorate EAM in mice through CD11b-positive cells, cytokines, and MMP-9 expression.
Expert Opinion on Investigational Drugs | 2014
Yuko Tada; Masahito Ogawa; Ryo Watanabe; Hirofumi Zempo; Chisato Takamura; Jun-ichi Suzuki; Takashi Dan; Toshio Miyata; Mitsuaki Isobe; Issei Komuro
Objective: Mechanisms of cardiac dysfunction in myocarditis have not been fully elucidated. Though it remains controversial whether angiogenesis is beneficial or harmful in inflammatory disease, significant vascular destruction might possibly impair cardiac function in myocarditis. The prolyl hydroxylase domain-containing protein (PHD) inhibitor is a potential drug for promoting angiogenesis as it stabilizes hypoxia inducible transcription factor (HIF). The authors examine whether the PHD inhibitor TM6008 could affect cardiac function by promoting angiogenesis in experimental autoimmune myocarditis (EAM). Methods: EAM was induced on BALB/c mice by immunizing them with a synthesized α myosin heavy-chain peptide. Every day, 200 mg/kg of TM6008 or vehicle was administered orally. Results: TM6008 improved left ventricular ejection fraction significantly on the 21st day of EAM. Though TM6008 did not affect the severity of myocardial cell infiltration, it tended to reduce cardiac fibrosis. Immunohistochemistry showed that CD31-positive blood vessels were preserved in the TM6008 group compared to the control group. Immunoblotting revealed that TM6008 increased the expression of HIF-1α, HIF-2α and vascular endothelial growth factor in myocarditis. Conclusion: Inhibition of PHD could ameliorate cardiac dysfunction in EAM, partially through promoting neovascularization. Relief of tissue hypoxia via neovascularization could improve cardiac function in myocarditis.
Journal of Cardiology | 2016
Chisato Takamura; Jun-ichi Suzuki; Masahito Ogawa; Ryo Watanabe; Yuko Tada; Yasuhiro Maejima; Hiroshi Akazawa; Issei Komuro; Mitsuaki Isobe
BACKGROUND The renin angiotensin system (RAS) plays an important role in the pathogenesis of cardiovascular diseases and inflammation. Myocarditis is an inflammatory disease of the heart, and the role of the RAS in its pathophysiology is unknown. Because the direct renin inhibitor, aliskiren, is thought to block RAS completely, we investigated the cardioprotective effect of aliskiren in mice with experimental autoimmune myocarditis (EAM). METHODS A cardiac α-myosin heavy chain peptide was injected in mice on days 0 and 7. Aliskiren 25mg/kg per day (n=10) or vehicle (n=10) was administered to EAM mice starting on day 0 and the animals were killed on day 21. RESULTS Aliskiren significantly prevented the progression of left ventricular wall thickening in EAM hearts compared to the vehicle-treated group. Histologically, the inflammatory cell infiltration and fibrosis area ratios in the aliskiren-treated group were lower than that in the vehicle-treated group. Immunohistochemistry revealed that aliskiren suppressed CD4 positive cell infiltration in EAM hearts compared to vehicle. Moreover, aliskiren decreased mRNA levels of interleukin (IL)-2, interferon-γ, tumor necrosis factor-α, and collagen 1. In vitro study showed that aliskiren inhibited T cell proliferation and IL-2 production induced by myosin stimulation. CONCLUSION Our results suggest that aliskiren ameliorates EAM by suppressing T-cell activation and inflammatory cytokines, and has potential as a treatment for myocarditis.
Internal Medicine | 2018
Tetsuo Yamaguchi; Masahiro Terashima; Chisato Takamura; Hironobu Sakurai; Kiyotoshi Ooishi; Tomoya Yoshizaki; Junji Yamaguchi; Sadahiro Hijikata; Takamasa Iwai; Yuichiro Sagawa; Keita Watanabe; Ryoichi Miyazaki; Ryo Masuda; Naoyuki Miwa; Masahiro Sekigawa; Nobuhiro Hara; Yasutoshi Nagata; Takamichi Miyamoto; Toru Obayashi; Toshihiro Nozato
A 55-year-old man presented with dyspnea, edema, and appetite loss. He had undergone coronary artery bypass grafting 8 years previously. He had jugular venous distention and Kussmauls sign. Contrast-enhanced cardiac magnetic resonance imaging (CMRI) demonstrated an intrapericardial mass compressing the right ventricular (RV) cavity. T1- and T2-weighted black-blood images showed a mass with heterogeneous high signal intensity and a thick and dark rim. The mass was considered to be a chronic hematoma. After pericardiotomy with surgical removal of the hematoma, CMRI showed the marked improvement of the RV function. Late intrapericardial hematoma is rare and CMRI is useful for making a differential diagnosis.
Circulation | 2012
Chisato Takamura; Hirokazu Ohhigashi; Yusuke Ebana; Mitsuaki Isobe
Japanese Circulation Journal-english Edition | 2009
Takamichi Miyamoto; Taeko Kozu; Masahito Suzuki; Mariko Kawasaki; Shingo Watanabe; Chisato Takamura; Atsushi Suzuki; Hiroyuki Okada; Eijirou Hattori; Yasuteru Yamauchi; Tohru Obayashi; Mitsuaki Isobe
Japanese Circulation Journal-english Edition | 2007
Yasuteru Yamauchi; Yukio Sekiguchi; Atsushi Suzuki; Koji Higuchi; Shigeki Kusa; Chisato Takamura; Hiroto Kano; Akiko Ooyama; Takaaki Miyamaoto; Tohru Obayashi; Akihiro Niwa; Kazutaka Aonuma; Mitsuaki Isobe
Immunology‚ Endocrine & Metabolic Agents in Medicinal Chemistry | 2013
Hirofumi Zempo; Jun-ichi Suzuki; Masahito Ogawa; Ryo Watanabe; Yuko Tada; Chisato Takamura; Mitsuaki Isobe
Journal of Cardiac Failure | 2012
Daisuke Tezuka; Go Haraguchi; Takashi Ishihara; Chisato Takamura; Jun-ichi Suzuki; Mitsuaki Isobe
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National Institute of Advanced Industrial Science and Technology
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