Publikasi Scopus 2024 per tanggal 31 Mei 2024 (409 artikel)

Tanaka T.; Sasaki N.; Krisnanda A.; Shinohara M.; Amin H.Z.; Horibe S.; Ito K.; Iwaya M.; Fukunaga A.; Hirata K.-I.; Rikitake Y.
Tanaka, Toru (57371497600); Sasaki, Naoto (22981407200); Krisnanda, Aga (57219731136); Shinohara, Masakazu (7201444851); Amin, Hilman Zulkifli (56217714300); Horibe, Sayo (7005880000); Ito, Ken (58817848700); Iwaya, Motoaki (7005536924); Fukunaga, Atsushi (7006390864); Hirata, Ken-Ichi (57204015476); Rikitake, Yoshiyuki (6701822639)
57371497600; 22981407200; 57219731136; 7201444851; 56217714300; 7005880000; 58817848700; 7005536924; 7006390864; 57204015476; 6701822639
Novel UV-B Phototherapy With a Light-Emitting Diode Device Prevents Atherosclerosis by Augmenting Regulatory T-Cell Responses in Mice
2024
Journal of the American Heart Association
13
2
e031639
0
Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan; Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan; Division of Molecular Epidemiology, Kobe University Graduate School of Medicine, Kobe, Japan; The Integrated Center for Mass Spectrometry, Kobe University Graduate School of Medicine, Kobe, Japan; Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan; Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; Department of Materials Science and Engineering, Meijo University, Nagoya, Japan; Department of Dermatology, Division of Medicine for Function and Morphology of Sensory Organs, Faculty of Medicine, Osaka Medical and Pharmaceutical University, Osaka, Takatsuki, Japan
Tanaka T., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan; Sasaki N., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan, Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan; Krisnanda A., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan; Shinohara M., Division of Molecular Epidemiology, Kobe University Graduate School of Medicine, Kobe, Japan, The Integrated Center for Mass Spectrometry, Kobe University Graduate School of Medicine, Kobe, Japan; Amin H.Z., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan, Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; Horibe S., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan; Ito K., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan; Iwaya M., Department of Materials Science and Engineering, Meijo University, Nagoya, Japan; Fukunaga A., Department of Dermatology, Division of Medicine for Function and Morphology of Sensory Organs, Faculty of Medicine, Osaka Medical and Pharmaceutical University, Osaka, Takatsuki, Japan; Hirata K.-I., Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan; Rikitake Y., Laboratory of Medical Pharmaceutics, Kobe Pharmaceutical University, Kobe, Japan
BACKGROUND: Ultraviolet B (UV-B) irradiation is an effective treatment for human cutaneous disorders and was shown to reduce experimental atherosclerosis by attenuating immunoinflammatory responses. The aim of this study was to clarify the effect of specific wavelengths of UV-B on atherosclerosis and the underlying mechanisms focusing on immunoinflammatory responses. METHODS AND RESULTS: Based on light-emitting diode technology, we developed novel devices that can emit 282 nm UV-B, which we do not receive from natural sunlight, 301 nm UV-B, and clinically available 312 nm UV-B. We irradiated 6-week-old male atherosclerosis-prone Apoe−/− (apolipoprotein E-deficient) mice with specific wavelengths of UV-B and evaluated atherosclerosis and immunoinflammatory responses by performing histological analysis, flow cytometry, biochemical assays, and liquid chro-matography/mass spectrometry-based lipidomics. Irradiation of 282 nm UV-B but not 301 or 312 nm UV-B significantly reduced the development of aortic root atherosclerotic plaques and plaque inflammation. This atheroprotection was associated with specifically augmented immune responses of anti-inflammatory CD4+ Foxp3 (forkhead box P3)+ regulatory T cells in lymphoid tissues, whereas responses of other immune cells were not substantially affected. Analysis of various lipid mediators revealed that 282 nm UV-B markedly increased the ratio of proresolving to proinflammatory lipid mediators in the skin. CONCLUSIONS: We demonstrated that 282 nm UV-B irradiation effectively reduces aortic inflammation and the development of atherosclerosis by systemically augmenting regulatory T-cell responses and modulating the balance between proresolving and proinflammatory lipid mediators in the skin. Our findings indicate that a novel 282 nm UV-B phototherapy could be an attractive approach to treat atherosclerosis. © 2024 The Authors.
atherosclerosis; immunology; inflammation; ultraviolet B
Animals; Apolipoproteins E; Atherosclerosis; Humans; Inflammation; Lipids; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Plaque, Atherosclerotic; T-Lymphocytes, Regulatory; Ultraviolet Therapy; 25 hydroxyvitamin D; butorphanol; calcitriol; chemokine receptor CCR4; concanavalin A; cytokine; docosahexaenoic acid; eosin; gamma interferon; hematoxylin; high density lipoprotein cholesterol; icosapentaenoic acid; interleukin 10; interleukin 17; interleukin 4; medetomidine; midazolam; prostaglandin E2; transcription factor FOXP3; transforming growth factor beta; triacylglycerol; apolipoprotein E; lipid; animal experiment; animal model; animal tissue; aortic sinus; Article; assay; atherosclerosis; biochemical parameters; CD4+ T lymphocyte; cholesterol blood level; cytokine assay; enzyme linked i
Suzuken Memorial Foundation; Takeda Science Foundation, TSF; Pfizer Japan; Novartis Japan; Japan Society for the Promotion of Science, JSPS, (18K08088, 21K08042); Astellas Pharma; SENSHIN Medical Research Foundation, SMRF
This work was supported by Japan Society for the Promotion of Science (JSPS) KAKENHI Grant Numbers 18K08088 (N.S.) and 21K08042 (N.S.) and research grants from Pfizer Japan Inc. (Y.R.), Astellas Pharma Inc. (Y.R.), Novartis Pharma K.K. (N.S.), Takeda Science Foundation (N.S.), Suzuken Memorial Foundation (N.S.), and Senshin Medical Research Foundation (N.S.).
American Heart Association Inc.
20479980
38214259
Article
Q1
2079
1229