6 results on '"Hirata, Yoichiro"'
Search Results
2. Heparin cofactor II protects against angiotensin II-induced cardiac remodeling via attenuation of oxidative stress in mice.
- Author
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Sumitomo-Ueda, Yuka, Aihara, Ken-ichi, Ise, Takayuki, Yoshida, Sumiko, Ikeda, Yasumasa, Uemoto, Ryoko, Yagi, Shusuke, Iwase, Takashi, Ishikawa, Kazue, Hirata, Yoichiro, Akaike, Masashi, Sata, Masataka, Kato, Shigeaki, and Matsumoto, Toshio
- Abstract
Heparin cofactor II (HCII), a serine protease inhibitor, inhibits tissue thrombin action after binding with dermatan sulfate proteoglycans in the extracellular matrix of the vascular system. We previously reported that heterozygous HCII-deficient (HCII(+/-)) humans and mice demonstrate acceleration of vascular remodeling, including atherosclerosis. However, the action of HCII on cardiac remodeling never has been determined. HCII(+/+) and HCII(+/-) mice at age 25 weeks were infused with angiotensin II (Ang II; 2.0 mg/kg/d) for 2 weeks by an osmotic mini-pump. Echocardiography revealed acceleration of cardiac concentric remodeling in HCII(+/-) mice and larger left atrial volume in HCII(+/-) mice than in HCII(+/+) mice. Histopathologic studies showed more prominent interstitial fibrosis in both the left atrium and left ventricle in HCII(+/-) mice than in HCII(+/+) mice. Daily urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and dihydroethidium-positive spots, indicating superoxide production in the myocardium, were markedly increased in Ang II-treated HCII(+/-) mice compared to those in HCII(+/+) mice. Cardiac gene expression levels of atrial natriuretic peptides and brain natriuretic peptides, members of the natriuretic peptide family, Nox 4, Rac-1, and p67(phox) as components of NAD(P)H oxidase, and transforming growth factor-beta1 and procollagen III were more augmented in HCII(+/-) mice than in HCII(+/+) mice. However, administration of human HCII protein attenuated all of those abnormalities in Ang II-treated HCII(+/-) mice. Moreover, human HCII protein supplementation almost abolished cardiac fibrosis in Ang II-treated HCII(+/+) mice. The results indicate that HCII has a protective role against Ang II-induced cardiac remodeling through suppression of the NAD(P)H oxidase-transforming growth factor-beta1 pathway. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
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3. Impact of Pathogenic FBN1 Variant Types on the Progression of Aortic Disease in Patients With Marfan Syndrome.
- Author
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Takeda, Norifumi, Inuzuka, Ryo, Maemura, Sonoko, Morita, Hiroyuki, Nawata, Kan, Fujita, Daishi, Taniguchi, Yuki, Yamauchi, Haruo, Yagi, Hiroki, Kato, Masayoshi, Nishimura, Hiroshi, Hirata, Yoichiro, Ikeda, Yuichi, Kumagai, Hidetoshi, Amiya, Eisuke, Hara, Hironori, Fujiwara, Takayuki, Akazawa, Hiroshi, Suzuki, Jun-ichi, and Imai, Yasushi
- Abstract
Supplemental Digital Content is available in the text. Background: Marfan syndrome can cause life-threatening aortic complications. We investigated the relationship between
FBN1 genotype and severe aortopathy (aortic root replacement, type A dissections, and related death). Methods: We evaluated 248 patients with pathogenic or likely pathogenicFBN1 variants. The variants were classified as haploinsufficient type (HI, n=93) or dominant-negative type (DN, n=155) based on their location and predicted amino acid alterations, and we examined the effects of theFBN1 genotype on severe aortic events (aortic root replacement, type A dissections, and related death). Results: The cumulative event-free probability was significantly lower in the HI group than in the DN group (adjusted hazard ratio, 2.1; 95% confidence interval, 1.4 -3.2;P <0.001). Male patients were at a greater than two-fold increased risk in both genotypes. In addition, after identifying deleterious variants among DN patients, we found that those with variants affecting or creating Cysteine residues and in-frame Deletion variants in exons 25–36 and 43–49 (DN-CD group) had a 6.3-fold higher risk compared with DN-nonCD patients (P <0.0001), which was comparable to or more deleterious than HI patients (P =0.062). Furthermore, DN-CD + HI patients had larger aortic root Z-scores than DN-nonCD patients (P <0.05 for <20 years;P <0.01 for 20–40 years), and males under 20 years old were more likely to develop aneurysms with higher rate of change in Z-score than females (P <0.001 in males;P =0.24 in females). Conclusions: DN-CD+HI patients should be monitored more carefully than DN-nonCD patients for rapid development of aortic root aneurysms. [ABSTRACT FROM AUTHOR]- Published
- 2018
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4. Impact of Pathogenic FBN1 Variant Types on the Progression of Aortic Disease in Patients With Marfan Syndrome.
- Author
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Takeda N, Inuzuka R, Maemura S, Morita H, Nawata K, Fujita D, Taniguchi Y, Yamauchi H, Yagi H, Kato M, Nishimura H, Hirata Y, Ikeda Y, Kumagai H, Amiya E, Hara H, Fujiwara T, Akazawa H, Suzuki JI, Imai Y, Nagai R, Takamoto S, Hirata Y, Ono M, and Komuro I
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Aortic Diseases complications, Aortic Diseases genetics, Child, Child, Preschool, Disease Progression, Female, Genes, Dominant, Haploinsufficiency, Humans, Male, Marfan Syndrome complications, Marfan Syndrome genetics, Middle Aged, Retrospective Studies, Severity of Illness Index, Young Adult, Aortic Diseases pathology, Fibrillin-1 genetics, Genomics methods, Marfan Syndrome pathology, Mutation
- Abstract
Background: Marfan syndrome can cause life-threatening aortic complications. We investigated the relationship between FBN1 genotype and severe aortopathy (aortic root replacement, type A dissections, and related death)., Methods: We evaluated 248 patients with pathogenic or likely pathogenic FBN1 variants. The variants were classified as haploinsufficient type (HI, n=93) or dominant-negative type (DN, n=155) based on their location and predicted amino acid alterations, and we examined the effects of the FBN1 genotype on severe aortic events (aortic root replacement, type A dissections, and related death)., Results: The cumulative event-free probability was significantly lower in the HI group than in the DN group (adjusted hazard ratio, 2.1; 95% confidence interval, 1.4 -3.2; P <0.001)., Conclusions: DN-CD+HI patients should be monitored more carefully than DN-nonCD patients for rapid development of aortic root aneurysms., (© 2018 American Heart Association, Inc.)
- Published
- 2018
- Full Text
- View/download PDF
5. Accelerated Cardiomyocyte Proliferation in the Heart of a Neonate With LEOPARD Syndrome-Associated Fatal Cardiomyopathy.
- Author
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Nakagama Y, Inuzuka R, Ichimura K, Hinata M, Takehara H, Takeda N, Kakiuchi S, Shiraga K, Asakai H, Shindo T, Hirata Y, Saitoh M, and Oka A
- Subjects
- Cardiomyopathies pathology, Female, Heart Failure diagnosis, Humans, Infant, Newborn, LEOPARD Syndrome diagnosis, Cardiomegaly pathology, Cell Proliferation physiology, Heart Failure pathology, LEOPARD Syndrome genetics, Myocytes, Cardiac pathology
- Published
- 2018
- Full Text
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6. Epicardial adipose tissue volume and adipocytokine imbalance are strongly linked to human coronary atherosclerosis.
- Author
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Shimabukuro M, Hirata Y, Tabata M, Dagvasumberel M, Sato H, Kurobe H, Fukuda D, Soeki T, Kitagawa T, Takanashi S, and Sata M
- Subjects
- Aged, Antigens, CD analysis, Antigens, Differentiation, Myelomonocytic analysis, CD11c Antigen analysis, Cholesterol, HDL blood, Coronary Artery Disease metabolism, Coronary Artery Disease pathology, Female, Humans, Logistic Models, Male, Middle Aged, Adipokines metabolism, Adipose Tissue pathology, Coronary Artery Disease etiology, Pericardium pathology
- Abstract
Objective: The impact of epicardial adipose tissue (EAT) over abdominal or overall adiposity on coronary artery disease (CAD) is currently unknown. We compared the association among EAT volume (EATV), cytokine/adipocytokine profiles in EAT and subcutaneous fat, and atherogenic CAD., Approach and Results: Paired samples were obtained from EAT and subcutaneous adipose tissue during elective cardiac surgery for CAD (n=50) or non-CAD (n=50). EATV was the sum of cross-sectional EAT areas, and visceral and subcutaneous fat areas were determined at the umbilicus level on computed tomography scans. CD68(+), CD11c(+), and CD206(+) cells were counted using immunohistochemical staining. Cytokine/adipocytokine expression was evaluated using quantitative real-time polymerase chain reaction. Multivariate analysis indicated that male sex, age, diabetes mellitus, high triglycerides, and low high-density lipoprotein cholesterol, and EATV index (EATV/body surface area, cm(3)/m(2)) were significant CAD predictors (corrected R(2)=0.401; P<0.001); visceral fat area, hypertension, smoking, low-density lipoprotein cholesterol (140 mg/dL [3.63 mmol/L]) or statin use were not predictors. The EATV index positively correlated with the CD68(+) and CD11c(+) cell numbers and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), interleukin-1β, and interleukin-1R expression; and negatively correlated with adiponectin expression in EAT. A multivariate analysis model, including CD68(+) cells and interleukin-1β, and adiponectin expression in EAT strongly predicted CAD (corrected R(2)=0.756; P<0.001)., Conclusions: EATV and macrophage and cytokine/adipocytokine signals in EAT strongly correlated with CAD. Our findings suggest that EATV and adipocytokine imbalance are strongly linked to human coronary atherosclerosis.
- Published
- 2013
- Full Text
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