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1. Fact-finding survey of doctors at the departments of pediatrics and pediatric surgery on the transition of patients with childhood-onset chronic disease from pediatric to adult healthcare

Author

Kikuchi, Ryota, primary, Sato, Iori, additional, Hirata, Yoichiro, additional, Sugiyama, Masahiko, additional, Iwasaki, Miwa, additional, Sekiguchi, Hiromi, additional, Sato, Atsushi, additional, Suzuki, Seigo, additional, Morisaki-Nakamura, Mayumi, additional, Kita, Sachiko, additional, Oka, Akira, additional, Kamibeppu, Kiyoko, additional, Ikeda, Mari, additional, and Kato, Motohiro, additional

Published
2023
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3. Relationship between high trait anxiety in 22q11.2 deletion syndrome and the difficulties in medical, welfare, and educational services

Author

Nakajima, Naomi, primary, Tanaka, Miho, additional, Kanehara, Akiko, additional, Morishima, Ryo, additional, Kumakura, Yousuke, additional, Ohkouchi, Noriko, additional, Hamada, Junko, additional, Ogawa, Tomoko, additional, Tamune, Hidetaka, additional, Nakahara, Mutsumi, additional, Mori, Shunsuke, additional, Ichihashi, Kayo, additional, Jinde, Seiichiro, additional, Kano, Yukiko, additional, Sakamoto, Ichiro, additional, Tanaka, Kyoko, additional, Hirata, Yoichiro, additional, Ohashi, Hirofumi, additional, Shinohara, Tokuko, additional, and Kasai, Kiyoto, additional

Published
2023
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8. Biodegradable Extremely-Small-Diameter Vascular Graft Made of Silk Fibroin can be Implanted in Mice

Author

Tanaka, Kimie, Fukuda, Daiju, Higashikuni, Yasutomi, Hirata, Yoichiro, Komuro, Issei, Saotome, Toshiki, Yamashita, Yoshihiro, Asakura, Tetsuo, and Sata, Masataka

Subjects
Mouse, Smooth muscle cells, Fibroin, Endothelial cells, fungi, Vascular graft
Abstract

Aim: Synthetic vascular grafts are widely used in surgical revascularization, mainly for medium- to large-sized vessels. However, synthetic grafts smaller than 6 mm in diameter are associated with a high incidence of thrombosis. In this study, we evaluated silk fibroin, a major protein of silk, with high biocompatibility and biodegradability, as a useful material for extremely-small-diameter vascular grafts. Methods: A small-sized (0.9 mm inner diameter) graft was braided from a silk fibroin thread. The right carotid arteries of 8- to 14-week-old male C57BL/6 mice were cut at the midpoint, and fibroin grafts (5- to 7-mm in length) were transplanted using a cuff technique with polyimide cuffs. The grafts were harvested at different time points and analyzed histologically. Results: CD31＋ endothelial cells had already started to proliferate at 2 weeks after implantation. At 4 weeks, neointima had formed with α-smooth muscle actin+ cells, and the luminal surface was covered with CD31＋endothelial cells. Mac3＋ macrophages were accumulated in the grafts. Graft patency was confirmed at up to 6 months after implantation. Conclusion: This mouse model of arterial graft implantation enables us to analyze the remodeling process and biocompatibility of extremely-small-diameter vascular grafts. Biodegradable silk fibroin might be applicable for further researches using genetically modified mice.

Published
2020

10. DPP-4阻害薬であるビルダグリプチンは、非糖尿病アポリポタンパク質E欠損マウスの内皮機能障害と動脈硬化形成を軽減する

Author

Aini, Kunduziayi, Fukuda, Daiju, Tanaka, Kimie, Higashikuni, Yasutomi, Hirata, Yoichiro, Yagi, Shusuke, Kusunose, Kenya, Yamada, Hirotsugu, Soeki, Takeshi, and Sata, Masataka

Subjects
Endothelial Dysfunction, Diabetes mellitus, DPP-4 inhibitors, Endothelial function, Atherosclerosis, GLP-1
Abstract

Dipeptidyl peptidase-4 (DPP-4) inhibitors are novel antidiabetic agents with possible vascular protection effects. Endothelial dysfunction is an initiation step in atherogenesis. The purpose of this study was to investigate whether vildagliptin (Vilda) attenuates the development of endothelial dysfunction and atherosclerotic lesions in nondiabetic apolipoprotein E-deficient (ApoE−/−) mice. Eight-week-old nondiabetic ApoE−/− mice fed a Western-type diet received Vilda (50 mg/kg/day) for 20 weeks or 8 weeks. After 20 weeks of treatment, Vilda administration reduced atherogenesis in the aortic arch as determined by en face Sudan IV staining compared with the vehicle group (P < 0.05). Vilda also reduced lipid accumulation (P < 0.05) and vascular cell adhesion molecule-1 (VCAM-1) expression (P < 0.05) and tended to decrease macrophage infiltration (P = 0.05) into atherosclerotic plaques compared with vehicle. After 8 weeks of treatment, endothelium-dependent vascular reactivity was examined. Vilda administration significantly attenuated the impairment of endothelial function in nondiabetic ApoE−/− mice compared with the vehicle group (P < 0.05). Vilda treatment did not alter metabolic parameters, including blood glucose level, in both study protocols. To investigate the mechanism, aortic segments obtained from wild-type mice were incubated with exendin-4 (Ex-4), a glucagon-like peptide-1 (GLP-1) analog, in the presence or absence of lipopolysaccharide (LPS). Ex-4 attenuated the impairment of endothelium-dependent vasodilation induced by LPS (P < 0.01). Furthermore, Ex-4 promoted phosphorylation of eNOS at Ser1177 which was decreased by LPS in human umbilical endothelial cells (P < 0.05). Vilda inhibited the development of endothelial dysfunction and prevented atherogenesis in nondiabetic ApoE−/− mice. Our results suggested that GLP-1-dependent amelioration of endothelial dysfunction is associated with the atheroprotective effects of Vilda.

Published
2019

12. Identification of Peripheral Blood Cells Infected with Epstein–Barr Virus: A Practical Method for Choosing the Initial Treatment for Post-Transplantation Lymphoproliferative Disease

Author

Ishibashi, Seijiro, primary, Nakano, Katsutoshi, additional, Urata, Susumu, additional, Nakagawa, Ryo, additional, Asakai, Hiroko, additional, Hirata, Yoichiro, additional, Hiwatari, Mitsuteru, additional, Imadome, Kenichi, additional, Ikemura, Masako, additional, and Inuzuka, Ryo, additional

Published
2021
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13. Poor Myocardial Compaction in a Patient with Recessive MYL2 Myopathy

Author

Tamamitsu, Ayaka Monoi, primary, Nakagama, Yu, additional, Domoto, Yukako, additional, Yoshida, Kenichi, additional, Ogawa, Seishi, additional, Hirono, Keiichi, additional, Shindo, Takahiro, additional, Ogawa, Yosuke, additional, Nakano, Katsutoshi, additional, Asakai, Hiroko, additional, Hirata, Yoichiro, additional, Matsui, Hikoro, additional, and Inuzuka, Ryo, additional

Published
2021
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15. P2Y12阻害薬チカグレロールはアポリポ蛋白E欠損マウスの血管障害を軽減して動脈硬化形成を抑制する

Author

Ganbaatar, Byambasuren, Fukuda, Daiju, Salim, Hotimah Masdan, Nishimoto, Sachiko, Tanaka, Kimie, Higashikuni, Yasutomi, Hirata, Yoichiro, Yagi, Shusuke, Soeki, Takeshi, and Sata, Masataka

Subjects
Inflammation, Ticagrelor, P2Y12, Endothelial function, Atherosclerosis
Abstract

Background and aims: Ticagrelor reduces cardiovascular events in patients with acute coronary syndrome (ACS). Recent studies demonstrated the expression of P2Y12 on vascular cells including endothelial cells, as well as platelets, and suggested its contribution to atherogenesis. We investigated whether ticagrelor attenuates vascular dysfunction and inhibits atherogenesis in apolipoprotein E-deficient (apoe-/-) mice. Methods: Eight-week-old male apoe-/- mice were fed a western-type diet (WTD) supplemented with 0.1% ticagrelor (approximately 120 mg/kg/day). Non-treated animals on WTD served as control. Atherosclerotic lesions were examined by en-face Sudan IV staining, histological analyses, quantitative RT-PCR analysis, and western blotting. Endothelial function was analyzed by acetylcholine-dependent vasodilation using aortic rings. Human umbilical vein endothelial cells (HUVEC) were used for in vitro experiments. Results: Ticagrelor treatment for 20 weeks attenuated atherosclerotic lesion progression in the aortic arch compared with control (p < 0.05). Ticagrelor administration for 8 weeks attenuated endothelial dysfunction (p < 0.01). Ticagrelor reduced the expression of inflammatory molecules such as vascular cell adhesion molecule-1, macrophage accumulation, and lipid deposition. Ticagrelor decreased the phosphorylation of JNK in the aorta compared with control (p < 0.05). Ticagrelor and a JNK inhibitor ameliorated impairment of endothelium-dependent vasodilation by adenosine diphosphate (ADP) in wild-type mouse aortic segments. Furthermore, ticagrelor inhibited the expression of inflammatory molecules which were promoted by ADP in HUVEC (p < 0.001). Ticagrelor also inhibited ADP-induced JNK activation in HUVEC (p < 0.05). Conclusions: Ticagrelor attenuated vascular dysfunction and atherogenesis through the inhibition of inflammatory activation of endothelial cells. These effects might be a potential mechanism by which ticagrelor decreases cardiovascular events in patients with ACS.

Published
2018

17. The Radioprotective 105/MD-1 Complex Contributes to Diet-Induced Obesity and Adipose Tissue Inflammation

Author

Watanabe, Yasuharu, Nakamura, Tomoya, Ishikawa, Sho, Fujisaka, Shiho, Usui, Isao, Tsuneyama, Koichi, Ichihara, Yoshinori, Wada, Tsutomu, Hirata, Yoichiro, Suganami, Takayoshi, Izaki, Hirofumi, Akira, Shizuo, Miyake, Kensuke, Kanayama, Hiro-omi, Shimabukuro, Michio, Sata, Masataka, Sasaoka, Toshiyasu, Ogawa, Yoshihiro, Tobe, Kazuyuki, Takatsu, Kiyoshi, and Nagai, Yoshinori

Published
2012
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19. Toward co‐production of research in 22q11.2 deletion syndrome: Research needs from the caregiver's perspective

Author

Tamune, Hidetaka, primary, Kumakura, Yousuke, additional, Morishima, Ryo, additional, Kanehara, Akiko, additional, Tanaka, Miho, additional, Okochi, Noriko, additional, Nakajima, Naomi, additional, Hamada, Junko, additional, Ogawa, Tomoko, additional, Nakahara, Mutsumi, additional, Jinde, Seiichiro, additional, Kano, Yukiko, additional, Tanaka, Kyoko, additional, Hirata, Yoichiro, additional, Oka, Akira, additional, and Kasai, Kiyoto, additional

Published
2020
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24. Neonatal Enterovirus Myocarditis: A Case Report

Author

Yamagata, Tomosato, primary, Shindo, Takahiro, additional, Shiraga, Kazuhiro, additional, Asakai, Hiroko, additional, Hirata, Yoichiro, additional, Inuzuka, Ryo, additional, Kaneko, Mei, additional, Takanashi, Sayaka, additional, Mizuguchi, Masashi, additional, Fujimoto, Tsuguto, additional, and Oka, Akira, additional

Published
2019
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25. Telmisartan ameliorates insulin sensitivity by activating the AMPK/SIRT1 pathway in skeletal muscle of obese db/db mice

Author

Shiota Asuka, Shimabukuro Michio, Fukuda Daiju, Soeki Takeshi, Sato Hiromi, Uematsu Etsuko, Hirata Yoichiro, Kurobe Hirotsugu, Maeda Norikazu, Sakaue Hiroshi, Masuzaki Hiroaki, Shimomura Iichiro, and Sata Masataka

Subjects
Adiponectin, AMP-activated protein kinase, Obesity, Peroxisome proliferator-activated receptor-γ, SIRT1, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background Telmisartan is a well-established angiotensin II type 1 receptor blocker that improves insulin sensitivity in animal models of obesity and insulin resistance, as well as in humans. Telmisartan has been reported to function as a partial agonist of the peroxisome proliferator-activated receptor (PPAR) γ, which is also targeted by the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase (SIRT1). Here, we investigated the pathways through which telmisartan acts on skeletal muscle, in vitro as well as in vivo. Methods Nine-week-old male db/db mice were fed a 60% high-fat diet, with orally administrated either vehicle (carboxymethyl-cellulose, CMC), 5 mg/kg telmisartan, or 5 mg/kg telmisartan and 1 mg/kg GW9662, a selective irreversible antagonist of PPARγ, for 5 weeks. Effects of telmisartan on Sirt1 mRNA, AMPK phosphorylation, and NAD+/NADH ratio were determined in C2C12 cultured myocytes. Results and discussion Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4. Conclusions Our results indicate that telmisartan acts through a PPARγ-independent pathway, but at least partially exerts its effects by acting directly on skeletal muscle AMPK/SIRT1 pathways.

Published
2012
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26. Gender disparities in the association between epicardial adipose tissue volume and coronary atherosclerosis: A 3-dimensional cardiac computed tomography imaging study in Japanese subjects

Author

Dagvasumberel Munkhbaatar, Shimabukuro Michio, Nishiuchi Takeshi, Ueno Junji, Takao Shoichiro, Fukuda Daiju, Hirata Yoichiro, Kurobe Hirotsugu, Soeki Takeshi, Iwase Takashi, Kusunose Kenya, Niki Toshiyuki, Yamaguchi Koji, Taketani Yoshio, Yagi Shusuke, Tomita Noriko, Yamada Hirotsugu, Wakatsuki Tetsuzo, Harada Masafumi, Kitagawa Tetsuya, and Sata Masataka

Subjects
Atherosclerosis, Gender difference, Epicardial adipose tissue, Obesity, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background Growing evidence suggests that epicardial adipose tissue (EAT) may contribute to the development of coronary artery disease (CAD). In this study, we explored gender disparities in EAT volume (EATV) and its impact on coronary atherosclerosis. Methods The study population consisted of 90 consecutive subjects (age: 63 ± 12 years; men: 47, women: 43) who underwent 256-slice multi-detector computed tomography (MDCT) coronary angiography. EATV was measured as the sum of cross-sectional epicardial fat area on CT images, from the lower surface of the left pulmonary artery origin to the apex. Subjects were segregated into the CAD group (coronary luminal narrowing > 50%) and non-CAD group. Results EATV/body surface area (BSA) was higher among men in the CAD group than in the non-CAD group (62 ± 13 vs. 33 ± 10 cm3/m2, p < 0.0001), but did not differ significantly among women in the 2 groups (49 ± 18 vs. 42 ± 9 cm3/m2, not significant). Multivariate logistic analysis showed that EATV/BSA was the single predictor for >50% coronary luminal narrowing in men (p < 0.0001). Predictors excluded were age, body mass index, hypertension, diabetes mellitus, and hyperlipidemia. Conclusions Increased EATV is strongly associated with coronary atherosclerosis in men.

Published
2012
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27. Toll‐Like Receptor 9 Plays a Pivotal Role in Angiotensin II–Induced Atherosclerosis

Author

Fukuda, Daiju, primary, Nishimoto, Sachiko, additional, Aini, Kunduziayi, additional, Tanaka, Atsushi, additional, Nishiguchi, Tsuyoshi, additional, Kim‐Kaneyama, Joo‐ri, additional, Lei, Xiao‐Feng, additional, Masuda, Kiyoshi, additional, Naruto, Takuya, additional, Tanaka, Kimie, additional, Higashikuni, Yasutomi, additional, Hirata, Yoichiro, additional, Yagi, Shusuke, additional, Kusunose, Kenya, additional, Yamada, Hirotsugu, additional, Soeki, Takeshi, additional, Imoto, Issei, additional, Akasaka, Takashi, additional, Shimabukuro, Michio, additional, and Sata, Masataka, additional

Published
2019
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29. DPP-4阻害薬のひとつリナグリプチンは，正常血糖アポリポ蛋白E欠損マウスにおける血管内皮機能を改善し，動脈硬化を抑制する

Author

Salim, Hotimah Masdan, Fukuda, Daiju, Higashikuni, Yasutomi, Tanaka, Kimie, Hirata, Yoichiro, Yagi, Shusuke, Soeki, Takeshi, Shimabukuro, Michio, and Sata, Masataka

Subjects
Inflammation, Oxidative stress, DPP-4 inhibitor, Endothelial function, Linagliptin, GLP-1
Abstract

Background: Dipeptidyl peptidase-4 (DPP-4) inhibitors have vasoprotective effects. This study investigated whether a recently approved DPP-4 inhibitor, linagliptin (Lina), suppresses atherogenesis in non-diabetic apolipoprotein-E deficient (ApoE−/−) mice, and examined its effects on endothelial function. Methods and results: Lina (10 mg/kg/day) was administered orally to ApoE−/− mice for 20 weeks. Lina reduced atherogenesis without alteration of metabolic parameters including blood glucose level compared with control (P b 0.05). Results of immunohistochemical analyses and quantitative RT-PCR demonstrated that Lina significantly decreased inflammatory molecule expression and macrophage infiltration in the atherosclerotic aorta. Lina administration to ApoE−/− mice for 9 weeks ameliorated endothelium-dependent vasodilation compared with that in untreated mice. Plasma active glucagon-like peptide-1 (GLP-1) level was significantly higher in the treated group (P b 0.05). Exendin-4 (Ex-4), a GLP-1 analog, ameliorated endothelium-dependent vasodilation impaired by palmitic acid (PA) in wild-type mouse aortic segments. Ex-4 promoted phosphorylation of eNOSSer1177 and Akt, both of which were abrogated by PA, in human umbilical vein endothelial cells. In addition, Lina administration to ApoE−/− mice decreased oxidative stress, as determined by urinary 8-OHdG secretion and NADPH oxidase subunit expression in the abdominal aorta. Conclusion: Lina inhibited atherogenesis in non-diabetic ApoE−/− mice. Amelioration of endothelial dysfunction associated with a reduction of oxidative stress by GLP-1 contributes to the atheroprotective effects of Lina.

Published
2015

30. Noonan syndrome‐associated biallelic LZTR1 mutations cause cardiac hypertrophy and vascular malformations in zebrafish.

Author

Nakagama, Yu, Takeda, Norihiko, Ogawa, Seishi, Takeda, Hiroyuki, Furutani, Yoshiyuki, Nakanishi, Toshio, Sato, Tatsuyuki, Hirata, Yoichiro, Oka, Akira, and Inuzuka, Ryo

Subjects
CARDIAC hypertrophy, HUMAN abnormalities, NOONAN syndrome, PATHOLOGY, ZEBRA danio, RECESSIVE genes
Abstract

Background: Variants in the LZTR1 (leucine‐zipper‐like transcription regulator 1) gene (OMIM #600574) have been reported in recessive Noonan syndrome patients. In vivo evidence from animal models to support its causative role is lacking. Methods: By CRISPR‐Cas9 genome editing, we generated lztr1‐mutated zebrafish (Danio rerio). Analyses of histopathology and downstream signaling were performed to investigate the pathogenesis of cardiac and extracardiac abnormalities in Noonan syndrome. Results: A frameshift deletion allele was created in the zebrafish lztr1. Crosses of heterozygotes obtained homozygous lztr1 null mutants that modeled LZTR1 loss‐of‐function. Histological analyses of the model revealed ventricular hypertrophy, the deleterious signature of Noonan syndrome‐associated cardiomyopathy. Further, assessment for extracardiac abnormalities documented multiple vascular malformations, resembling human vascular pathology caused by RAS/MAPK activation. Due to spatiotemporal regulation of LZTR1, its downstream function was not fully elucidated from western blots of adult tissue. Conclusion: Our novel zebrafish model phenocopied human recessive Noonan syndrome and supported the loss‐of‐function mechanism of disease‐causing LZTR1 variants. The discovery of vascular malformations in mutants calls for the clinical follow‐up of patients to monitor for its emergence. The model will serve as a novel platform for investigating the pathophysiology linking RAS/MAPK signaling to cardiac and vascular pathology. [ABSTRACT FROM AUTHOR]

Published
2020
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31. Impact of Pathogenic FBN1 Variant Types on the Progression of Aortic Disease in Patients With Marfan Syndrome

Author

Takeda, Norifumi, primary, Inuzuka, Ryo, additional, Maemura, Sonoko, additional, Morita, Hiroyuki, additional, Nawata, Kan, additional, Fujita, Daishi, additional, Taniguchi, Yuki, additional, Yamauchi, Haruo, additional, Yagi, Hiroki, additional, Kato, Masayoshi, additional, Nishimura, Hiroshi, additional, Hirata, Yoichiro, additional, Ikeda, Yuichi, additional, Kumagai, Hidetoshi, additional, Amiya, Eisuke, additional, Hara, Hironori, additional, Fujiwara, Takayuki, additional, Akazawa, Hiroshi, additional, Suzuki, Jun-ichi, additional, Imai, Yasushi, additional, Nagai, Ryozo, additional, Takamoto, Shinichi, additional, Hirata, Yasunobu, additional, Ono, Minoru, additional, and Komuro, Issei, additional

Published
2018
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32. Accelerated Cardiomyocyte Proliferation in the Heart of a Neonate With LEOPARD Syndrome-Associated Fatal Cardiomyopathy

Author

Nakagama, Yu, primary, Inuzuka, Ryo, additional, Ichimura, Kayoko, additional, Hinata, Munetoshi, additional, Takehara, Hiroki, additional, Takeda, Norihiko, additional, Kakiuchi, Satsuki, additional, Shiraga, Kazuhiro, additional, Asakai, Hiroko, additional, Shindo, Takahiro, additional, Hirata, Yoichiro, additional, Saitoh, Makiko, additional, and Oka, Akira, additional

Published
2018
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35. The twenty-four army system and the fubing system of the Western Wei and Northern Zhou

Author

HIRATA, Yoichiro

Subjects
郷兵, 部族解散, 鄉兵, 乡兵, 府兵制, 親信, 二十四军, 亲信, 二十四軍
Abstract

The fubing system that was a driving force in the creation of Sui and Tang dynasties is generally thought to have begun with the twenty-four army system of the Western Wei, and its military power too have been composed of local militias of Han people in Western Wei and Northern Zhou during which the influx of warriors of the northern Xianbei peoples were not numerous. Nonetheless, the term fubing zhi, the fubing system, is not found in contemporary sources, and was invented in a later period. Tracing the fubing system back to the Western Wei is also nothing more than a distortion created by later hands. The local military organizations that comprised the military force of the twenty-four army system were both chronologically, geographically, and ethnically extremely diverse, and the local Han militias of Guanlong 關隴 were no more than one part of it. In the Western Wei and Northern Zhou levies of military service were generally imposed on households, but they resorted to having the local gentry organize military bands and thereby continued the selection and implementation of a method of operating as a pseudo-tribal militia. In addition the existence of a unique system of groups of close advisers, called qinxhin 親信 and kuzhen 庫眞, whose lineages could be traced to the inner officers of Northern Wei court, made it possible to control the vast military organization that was the twenty-four army system. Judging from these special characteristics, the twenty-four-army system can be understood as a pseudo-tribal militia system that was supported by the traditions of the Xianbei. In this regard, it should be positioned in the historical context as a military system located precisely within the lineage of the nomadic military systems such as the twenty-four chiefs of the Xiongnu and of the Mongol thousand-household system. The imperial edict of the tenth year of Kaihuang, which was promulgated the year after Sui destroyed the Chen, has been taken as revolutionary in creating the ground-breaking fubing system, but in actuality, the purpose of the edict was the transfer and settling of military groups who had served for years in Guanzhong, and their essential character as pseudo-Xiangbei tribal militia was maintained thereafter. A common element underlay both the purpose of the imperial edict of the tenth year of the Kaihuang reign and the Northern-Wei policy of dismantling the tribe-centered state, and in order to decipher this reality, one must seek a point of view from which both can be mutually examined and compared.

Published
2011

36. Obesity-induced DNA released from adipocytes stimulates chronic adipose tissue inflammation and insulin resistance

Author

Nishimoto, Sachiko, primary, Fukuda, Daiju, additional, Higashikuni, Yasutomi, additional, Tanaka, Kimie, additional, Hirata, Yoichiro, additional, Murata, Chie, additional, Kim-Kaneyama, Joo-ri, additional, Sato, Fukiko, additional, Bando, Masahiro, additional, Yagi, Shusuke, additional, Soeki, Takeshi, additional, Hayashi, Tetsuya, additional, Imoto, Issei, additional, Sakaue, Hiroshi, additional, Shimabukuro, Michio, additional, and Sata, Masataka, additional

Published
2016
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39. 肥満によって遊離する脂肪細胞由来のDNA断片が脂肪組織の炎症とインスリン抵抗性を引き起こす

Author

Nishimoto, Sachiko, Fukuda, Daiju, Higashikuni, Yasutomi, Tanaka, Kimie, Hirata, Yoichiro, Murata, Chie, Kim-Kaneyama, Joo-ri, Sato, Fukiko, Bando, Masahiro, Yagi, Shusuke, Soeki, Takeshi, Hayashi, Tetsuya, Imoto, Issei, Sakaue, Hiroshi, Shimabukuro, Michio, and Sata, Masataka

Subjects
cell-free DNA, 肥満, インスリン抵抗性, Toll-like receptor, inflammation, insulin resistance, 慢性炎症, macrophage, adipose tissue
Abstract

Obesity stimulates chronic inflammation in adipose tissue, which is associated with insulin resistance, although the underlying mechanism remains largely unknown. Here we showed that obesity-related adipocyte degeneration causes release of cell-free DNA (cfDNA), which promotes macrophage accumulation in adipose tissue via Toll-like receptor 9 (TLR9), originally known as a sensor of exogenous DNA fragments. Fat-fed obese wild-type mice showed increased release of cfDNA, as determined by the concentrations of single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) in plasma. cfDNA released from degenerated adipocytes promoted monocyte chemoattractant protein-1 (MCP-1) expression in wild-type macrophages, but not in TLR9-deficient (Tlr9−/−) macrophages. Fat-fed Tlr9−/− mice demonstrated reduced macrophage accumulation and inflammation in adipose tissue and better insulin sensitivity compared with wild-type mice, whereas bone marrow reconstitution with wild-type bone marrow restored the attenuation of insulin resistance observed in fat-fed Tlr9−/− mice. Administration of a TLR9 inhibitory oligonucleotide to fat-fed wild-type mice reduced the accumulation of macrophages in adipose tissue and improved insulin resistance. Furthermore, in humans, plasma ssDNA level was significantly higher in patients with computed tomography–determined visceral obesity and was associated with homeostasis model assessment of insulin resistance (HOMA-IR), which is the index of insulin resistance. Our study may provide a novel mechanism for the development of sterile inflammation in adipose tissue and a potential therapeutic target for insulin resistance.

Published
2016

41. Abstract 13438: Rivaroxaban, a Direct Factor Xa Inhibitor, Attenuates Neointima Formation after Mechanical Vascular Injury

Author

Hara, Tomoya, primary, Fukuda, Daiju, additional, Tanaka, Kimie, additional, Higashikuni, Yasutomi, additional, Hirata, Yoichiro, additional, Yagi, Shusuke, additional, Yamada, Hirotsugu, additional, Soeki, Takeshi, additional, Wakatsuki, Tetsuzo, additional, Shimabukuro, Michio, additional, and Sata, Masataka, additional

Published
2014
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43. Epicardial Adipose Tissue Volume and Adipocytokine Imbalance Are Strongly Linked to Human Coronary Atherosclerosis

Author

Shimabukuro, Michio, primary, Hirata, Yoichiro, additional, Tabata, Minoru, additional, Dagvasumberel, Munkhbaatar, additional, Sato, Hiromi, additional, Kurobe, Hirotsugu, additional, Fukuda, Daiju, additional, Soeki, Takeshi, additional, Kitagawa, Tetsuya, additional, Takanashi, Shuichiro, additional, and Sata, Masataka, additional

Published
2013
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44. Elevated concentrations of pentraxin 3 are associated with coronary plaque vulnerability

Author

Soeki, Takeshi, primary, Niki, Toshiyuki, additional, Kusunose, Kenya, additional, Bando, Sachiko, additional, Hirata, Yoichiro, additional, Tomita, Noriko, additional, Yamaguchi, Koji, additional, Koshiba, Kunihiko, additional, Yagi, Shusuke, additional, Taketani, Yoshio, additional, Iwase, Takashi, additional, Yamada, Hirotsugu, additional, Wakatsuki, Tetsuzo, additional, Akaike, Masashi, additional, and Sata, Masataka, additional

Published
2011
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46. Ezetimibe Monotherapy Ameliorates Vascular Function in Patients with Hypercholesterolemia Through Decreasing Oxidative Stress

Author

Kurobe, Hirotsugu, primary, Aihara, Ken-ichi, additional, Higashida, Mayuko, additional, Hirata, Yoichiro, additional, Nishiya, Masako, additional, Matsuoka, Yuki, additional, Kanbara, Tamotsu, additional, Nakayama, Taisuke, additional, Kinoshita, Hajime, additional, Sugano, Mikio, additional, Fujimoto, Eiki, additional, Kurobe, Ayako, additional, Sugasawa, Noriko, additional, Kitaichi, Takashi, additional, Akaike, Masashi, additional, Sata, Masataka, additional, Matsumoto, Toshio, additional, and Kitagawa, Tetsuya, additional

Published
2011
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48. Heparin Cofactor II Protects Against Angiotensin II-Induced Cardiac Remodeling Via Attenuation of Oxidative Stress in Mice

Author

Sumitomo-Ueda, Yuka, primary, Aihara, Ken-ichi, additional, Ise, Takayuki, additional, Yoshida, Sumiko, additional, Ikeda, Yasumasa, additional, Uemoto, Ryoko, additional, Yagi, Shusuke, additional, Iwase, Takashi, additional, Ishikawa, Kazue, additional, Hirata, Yoichiro, additional, Akaike, Masashi, additional, Sata, Masataka, additional, Kato, Shigeaki, additional, and Matsumoto, Toshio, additional

Published
2010
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49. Congenital Ventricular Aneurysm as an Unexpected Complication of Monomorphic Premature Ventricular Contractions

Author

Yagi, Shusuke, primary, Akaike, Masashi, additional, Fujimura, Mitsunori, additional, Kimura, Takehiko, additional, Nishiuchi, Takeshi, additional, Iwase, Takashi, additional, Aihara, Ken-ichi, additional, Yoshida, Sumiko, additional, Sumitomo-Ueda, Yuka, additional, Kusunose, Kenya, additional, Niki, Toshiyuki, additional, Yamaguchi, Koji, additional, Koshiba, Kunihiko, additional, Hirata, Yoichiro, additional, Dagvasumberel, Munkhbaatar, additional, Taketani, Yoshio, additional, Tomita, Noriko, additional, Yamada, Hirotsugu, additional, Soeki, Takeshi, additional, Wakatsuki, Tetsuzo, additional, Matsumoto, Toshio, additional, and Sata, Masataka, additional

Published
2010
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50. Bosentan Ameliorated Exercise-Induced Pulmonary Arterial Hypertension Complicated with Systemic Sclerosis

Author

Yagi, Shusuke, primary, Akaike, Masashi, additional, Iwase, Takashi, additional, Kusunose, Kenya, additional, Niki, Toshiyuki, additional, Yamaguchi, Koji, additional, Koshiba, Kunihiko, additional, Yoshida, Sumiko, additional, Sumitomo-Ueda, Yuka, additional, Aihara, Ken-ichi, additional, Hirata, Yoichiro, additional, Dagvasumberel, Munkhbaatar, additional, Taketani, Yoshio, additional, Tomita, Noriko, additional, Yamada, Hirotsugu, additional, Soeki, Takeshi, additional, Wakatsuki, Tetsuzo, additional, Matsumoto, Toshio, additional, and Sata, Masataka, additional

Published
2010
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