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1. Impact of Autophagy on Prognosis of Patients With Dilated Cardiomyopathy

Author

Kanamori, Hiromitsu, Yoshida, Akihiro, Naruse, Genki, Endo, Susumu, Minatoguchi, Shingo, Watanabe, Takatomo, Kawaguchi, Tomonori, Tanaka, Toshiki, Yamada, Yoshihisa, Takasugi, Nobuhiro, Ishihara, Takuma, Mikami, Atsushi, Miyazaki, Nagisa, Nishigaki, Kazuhiko, Minatoguchi, Shinya, Miyazaki, Tatsuhiko, and Okura, Hiroyuki

Published
2022
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3. Recombinant Antithrombin Attenuates Acute Respiratory Distress Syndrome in Experimental Endotoxemia

Author

Okamoto, Haruka, Muraki, Isamu, Okada, Hideshi, Tomita, Hiroyuki, Suzuki, Kodai, Takada, Chihiro, Wakayama, Yugo, Kuroda, Ayumi, Fukuda, Hirotsugu, Kawasaki, Yuki, Nishio, Ayane, Matsuo, Maho, Tamaoki, Yuto, Inagawa, Risa, Takashima, Shigeo, Taniguchi, Toshiaki, Suzuki, Akio, Suzuki, Keiko, Miyazaki, Nagisa, Kakino, Yoshinori, Yasuda, Ryu, Fukuta, Tetsuya, Kitagawa, Yuichiro, Miyake, Takahito, Doi, Tomoaki, Yoshida, Takahiro, Yoshida, Shozo, and Ogura, Shinji

Published
2021
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4. Neutrophil Elastase Damages the Pulmonary Endothelial Glycocalyx in Lipopolysaccharide-Induced Experimental Endotoxemia

Author

Suzuki, Kodai, Okada, Hideshi, Takemura, Genzou, Takada, Chihiro, Kuroda, Ayumi, Yano, Hirohisa, Zaikokuji, Ryogen, Morishita, Kentaro, Tomita, Hiroyuki, Oda, Kazumasa, Matsuo, Saori, Uchida, Akihiro, Fukuta, Tetsuya, Sampei, So, Miyazaki, Nagisa, Kawaguchi, Tomonori, Watanabe, Takatomo, Yoshida, Takahiro, Ushikoshi, Hiroaki, Yoshida, Shozo, Maekawa, Yoichi, and Ogura, Shinji

Published
2019
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6. Neutrophil Elastase Inhibition Ameliorates Endotoxin-induced Myocardial Injury Accompanying Degradation of Cardiac Capillary Glycocalyx

Author

Fukuta, Tetsuya, Okada, Hideshi, Takemura, Genzou, Suzuki, Kodai, Takada, Chihiro, Tomita, Hiroyuki, Suzuki, Akio, Oda, Kazumasa, Uchida, Akihiro, Matsuo, Saori, Fukuda, Hirotsugu, Yano, Hirohisa, Muraki, Isamu, Zaikokuji, Ryogen, Kuroda, Ayumi, Nishio, Ayane, Sampei, So, Miyazaki, Nagisa, Hotta, Yasuaki, Yamada, Noriaki, Watanabe, Takatomo, Morishita, Kentaro, Doi, Tomoaki, Yoshida, Takahiro, Ushikoshi, Hiroaki, Yoshida, Shozo, Maekawa, Yoichi, and Ogura, Shinji

Published
2020
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8. Brain-Specific Ultrastructure of Capillary Endothelial Glycocalyx and Its Possible Contribution for Blood Brain Barrier

Author

Ando, Yoshiaki, Okada, Hideshi, Takemura, Genzou, Suzuki, Kodai, Takada, Chihiro, Tomita, Hiroyuki, Zaikokuji, Ryogen, Hotta, Yasuaki, Miyazaki, Nagisa, Yano, Hirohisa, Muraki, Isamu, Kuroda, Ayumi, Fukuda, Hirotsugu, Kawasaki, Yuki, Okamoto, Haruka, Kawaguchi, Tomonori, Watanabe, Takatomo, Doi, Tomoaki, Yoshida, Takahiro, Ushikoshi, Hiroaki, Yoshida, Shozo, and Ogura, Shinji

Published
2018
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11. Serum syndecan-1 concentration in hospitalized patients with heart failure may predict readmission-free survival

Author

Kitagawa, Yuichiro, primary, Kawamura, Itta, additional, Suzuki, Keiko, additional, Okada, Hideshi, additional, Ishihara, Takuma, additional, Tomita, Hiroyuki, additional, Suzuki, Kodai, additional, Takada, Chihiro, additional, Sampei, So, additional, Kano, Soichiro, additional, Kondo, Kohei, additional, Asano, Hirotaka, additional, Wakayama, Yugo, additional, Kamidani, Ryo, additional, Kawasaki, Yuki, additional, Fukuda, Hirotsugu, additional, Nishio, Ayane, additional, Miyake, Takahito, additional, Fukuta, Tetsuya, additional, Yasuda, Ryu, additional, Oiwa, Hideaki, additional, Kakino, Yoshinori, additional, Miyazaki, Nagisa, additional, Watanabe, Takatomo, additional, Yoshida, Takahiro, additional, Doi, Tomoaki, additional, Suzuki, Akio, additional, Yoshida, Shozo, additional, Matsuo, Hitoshi, additional, and Ogura, Shinji, additional

Published
2021
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12. Possible mechanism for disposal of degenerative cardiomyocytes in human failing hearts: phagocytosis by a neighbour

Author

Takemura, Genzou, Onoue, Kenji, Nakano, Tomoya, Nakamura, Takuya, Sakaguchi, Yasuhiro, Tsujimoto, Akiko, Miyazaki, Nagisa, Watanabe, Takatomo, Kanamori, Hiromitsu, Okada, Hideshi, Kawasaki, Masanori, Fujiwara, Takako, Fujiwara, Hisayoshi, and Saito, Yoshihiko

Subjects
Phagocytosis, Cardiomyopathy, Ultrastructure, Chemotherapy, Endomyocardial biopsy, Case Report, Heart failure, Case Reports
Abstract

The index case was a 51‐year‐old woman suffering from doxorubicin cardiomyopathy. In her endomyocardial biopsy specimen, we observed under electron microscopy six scenes in which degenerative cardiomyocytes were engulfed by neighbouring cardiomyocytes. The enclosed cardiomyocytes appeared more degenerative than the enclosing ones in every pair: the myofibrils were more severely damaged. At more degenerative stages, some desmosomes of the intercalated discs on the enclosed cardiomyocyte had disappeared. The membranes between the cardiomyocytes were occasionally disrupted, and there appeared to be sharing of cellular contents between the cells. One pair of such a phagocytosis‐like figure was observed in one case with 5‐fluorouracil cardiomyopathy (a 68‐year‐old man) among eight other chemotherapy‐induced cardiomyopathies but none among 30 non‐drug‐induced dilated cardiomyopathies. The findings suggest a mechanism for disposal of degenerative cardiomyocytes in human failing hearts: phagocytosis by a neighbour, although alternative interpretations remain (e.g. giant autophagic vacuoles or two cardiomyocytes with degenerative intercalated discs).

Published
2018

13. Endothelial Glycocalyx Disorders May Be Associated With Extended Inflammation During Endotoxemia in a Diabetic Mouse Model

Author

Sampei, So, primary, Okada, Hideshi, additional, Tomita, Hiroyuki, additional, Takada, Chihiro, additional, Suzuki, Kodai, additional, Kinoshita, Takamasa, additional, Kobayashi, Ryo, additional, Fukuda, Hirotsugu, additional, Kawasaki, Yuki, additional, Nishio, Ayane, additional, Yano, Hirohisa, additional, Muraki, Isamu, additional, Fukuda, Yohei, additional, Suzuki, Keiko, additional, Miyazaki, Nagisa, additional, Watanabe, Takatomo, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Suzuki, Akio, additional, Yoshida, Shozo, additional, Kushimoto, Shigeki, additional, and Ogura, Shinji, additional

Published
2021
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14. Ultrastructural alteration of pulmonary tissue under conditions of high oxygen concentration

Author

Yano, Hirohisa, Kuroda, Ayumi, Okada, Hideshi, Tomita, Hiroyuki, Suzuki, Kodai, Takada, Chihiro, Fukuda, Hirotsugu, Kawasaki, Yuki, Muraki, Isamu, Wakayama, Yugo, Kano, Soichiro, Tamaoki, Yuto, Nishio, Ayane, Inagawa, Risa, Sampei, So, Kamidani, Ryo, Kakino, Yoshinori, Yasuda, Ryu, Kitagawa, Yuichiro, Fukuta, Tetsuya, Miyake, Takahito, Kanda, Norihide, Miyazaki, Nagisa, Doi, Tomoaki, Yoshida, Takahiro, Suzuki, Akio, Yoshida, Shozo, and Ogura, Shinji

Subjects
Original Article
Abstract

Objective: To determine the structure of pulmonary tissue under conditions of high oxygen concentration. Methods: Ten-week-old C57BL male mice and control mice were exposed to 100% oxygen and to room air for 72 hours, respectively. To follow the progression of lesions, the mice were sacrificed at 6, 12, 24, 48, and 72 hours after 100% oxygen administration. Lung specimens obtained from these mice underwent morphologic analysis and immunofluorescence studies. We used scanning and transmission electron microscopy to determine the ultrastructure of the pulmonary capillaries, including the endothelial glycocalyx. To visualize the endothelial glycocalyx, we performed lanthanum nitrate staining. Results: The survival rate of the 100% oxygen administration group was 5% (2/40) and that of the control group was 100%. Perivascular cavity enlargement was detected 12 hours after 100% oxygen administration and expanded over time. Ultrastructural analysis using electron microscopy revealed collapsed alveoli and pulmonary capillary wall and alveolar wall thickening in the 100% oxygen group. The pulmonary capillary endothelial glycocalyx was injured in the 100% oxygen group. The perivascular cavity decreased in mice that were returned to room air after 48 hours of 100% oxygen administration. Conclusion: High-concentration oxygen causes perivascular cavity enlargement; this is thought to be a special characteristic of high oxygen damage. In addition, high-concentration oxygen may be involved in pulmonary endothelial glycocalyx injury.

Published
2020

15. Recombinant thrombomodulin protects against LPS‐induced acute respiratory distress syndrome via preservation of pulmonary endothelial glycocalyx

Author

Suzuki, Kodai, primary, Okada, Hideshi, additional, Takemura, Genzou, additional, Takada, Chihiro, additional, Tomita, Hiroyuki, additional, Yano, Hirohisa, additional, Muraki, Isamu, additional, Zaikokuji, Ryogen, additional, Kuroda, Ayumi, additional, Fukuda, Hirotsugu, additional, Nishio, Ayane, additional, Takashima, Shigeo, additional, Suzuki, Akio, additional, Miyazaki, Nagisa, additional, Fukuta, Tetsuya, additional, Yamada, Noriaki, additional, Watanabe, Takatomo, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Kumada, Keisuke, additional, Ushikoshi, Hiroaki, additional, Yoshida, Shozo, additional, and Ogura, Shinji, additional

Published
2020
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16. Vacuolated cardiomyocytes in human endomyocardial biopsy specimens

Author

Takemura, Genzou, primary, Onoue, Kenji, additional, Arimoto, Takanori, additional, Watanabe, Tetsu, additional, Tsujimoto, Akiko, additional, Takada, Chihiro, additional, Okada, Hideshi, additional, Nakano, Tomoya, additional, Sakaguchi, Yasuhiro, additional, Miyazaki, Nagisa, additional, Watanabe, Takatomo, additional, Kanamori, Hiromitsu, additional, Ogura, Shinji, additional, Saito, Yoshihiko, additional, Fujiwara, Takako, additional, Fujiwara, Hisayoshi, additional, and Hotta, Yasuaki, additional

Published
2020
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17. In situ nuclear DNA methylation in dilated cardiomyopathy: an endomyocardial biopsy study

Author

Watanabe, Takatomo, primary, Okada, Hideshi, additional, Kanamori, Hiromitsu, additional, Miyazaki, Nagisa, additional, Tsujimoto, Akiko, additional, Takada, Chihiro, additional, Suzuki, Kodai, additional, Naruse, Genki, additional, Yoshida, Akihiro, additional, Nawa, Takahide, additional, Tanaka, Toshiki, additional, Kawasaki, Masanori, additional, Ito, Hiroyasu, additional, Ogura, Shinji, additional, Okura, Hiroyuki, additional, Fujiwara, Takako, additional, Fujiwara, Hisayoshi, additional, and Takemura, Genzou, additional

Published
2020
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18. Neutrophil Elastase Inhibition Ameliorates Endotoxin-induced Myocardial Injury Accompanying Degradation of Cardiac Capillary Glycocalyx

Author

Fukuta, Tetsuya, primary, Okada, Hideshi, additional, Takemura, Genzou, additional, Suzuki, Kodai, additional, Takada, Chihiro, additional, Tomita, Hiroyuki, additional, Suzuki, Akio, additional, Oda, Kazumasa, additional, Uchida, Akihiro, additional, Matsuo, Saori, additional, Fukuda, Hirotsugu, additional, Yano, Hirohisa, additional, Muraki, Isamu, additional, Zaikokuji, Ryogen, additional, Kuroda, Ayumi, additional, Nishio, Ayane, additional, Sampei, So, additional, Miyazaki, Nagisa, additional, Hotta, Yasuaki, additional, Yamada, Noriaki, additional, Watanabe, Takatomo, additional, Morishita, Kentaro, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Ushikoshi, Hiroaki, additional, Yoshida, Shozo, additional, Maekawa, Yoichi, additional, and Ogura, Shinji, additional

Published
2019
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19. Open Access

Author

Suzuki, Kodai, Okada, Hideshi, Takemura, Genzou, Takada, Chihiro, Kuroda, Ayumi, Yano, Hirohisa, Zaikokuji, Ryogen, Morishita, Kentaro, Tomita, Hiroyuki, Oda, Kazumasa, Matsuo, Saori, Uchida, Akihiro, Fukuta, Tetsuya, Sampei, So, Miyazaki, Nagisa, Kawaguchi, Tomonori, Watanabe, Takatomo, Yoshida, Takahiro, Ushikoshi, Hiroaki, Yoshida, Shozo, Maekawa, Yoichi, Ogura, Shinji, Department of Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Department of Internal Medicine, Asahi University School of Dentistry, Department of Emergency and Disaster Medicine, Gifu University Graduate School of MedicineLaboratory of Molecular Biology, Department of Biofunctional Analysis, Gifu Pharmaceutical University, Department of Tumor Pathology, Gifu University Graduate School of Medicine, Department of Clinical Laboratory, Gifu University Hospital, and Department of Parasitology and Infectious Diseases, Gifu University Graduate School of MedicineDomain of Integrated Life Systems, Center for Highly Advanced Integration of Nano and Life Sciences (G-CHAIN), Gifu University

Subjects
0301 basic medicine, Lipopolysaccharides, medicine.medical_specialty, Lipopolysaccharide, Endothelium, Glycine, Granulocyte, Thrombomodulin, Glycocalyx, Pathology and Forensic Medicine, Proinflammatory cytokine, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Internal medicine, medicine, Animals, Survival rate, Lung, Mice, Knockout, Sulfonamides, biology, business.industry, Sivelestat, 030208 emergency & critical care medicine, Endotoxemia, 030104 developmental biology, medicine.anatomical_structure, Endocrinology, chemistry, Neutrophil elastase, biology.protein, business, Leukocyte Elastase
Abstract

Neutrophil elastase (NE) is necessary for effective sterilization of phagocytosed bacterial and fungal pathogens; however, NE increases alveolocapillary permeability and induces proinflammatory cytokine production in sepsis-induced acute respiratory distress syndrome. Under septic conditions, the pulmonary endothelial glycocalyx covering on the healthy endothelium surface is injured, but the contribution of NE to this injury remains unknown. Our aim was to examine whether NE-induced pulmonary endothelial injury is associated with endotoxemia. Lipopolysaccharide (LPS; 20 mg/kg) was injected intraperitoneally into 9- to 12-week-old granulocyte colony-stimulating factor knockout (G-CSFKO) mice, which harbor few neutrophils, and littermate control mice; in a second assay, mice were injected with the NE-inhibitor sivelestat (0.2 mg/kg) at 3, 6, 9, and 12 hours after LPS administration. Subsequently, vascular endothelial injury was evaluated through ultrastructural analysis. At 48 hours after LPS injection, survival rate was more than threefold higher among G-CSFKO than control mice, and degradation of both thrombomodulin and syndecan-1 was markedly attenuated in G-CSFKO compared with control mice. Ultrastructural analysis revealed attenuated vascular endothelial injury and clear preservation of the endothelial glycocalyx in G-CSFKO mice. Moreover, after LPS exposure, survival rate was approximately ninefold higher among sivelestat-injected mice than control mice, and sivelestat treatment potently preserved vascular endothelial structures and the endothelial glycocalyx. In conclusion, NE is associated with pulmonary endothelial injury under LPS-induced endotoxemic conditions.

Published
2018

20. Ultrastructural Evidence of Glycosphingolipid Degradation After Enzyme Replacement Therapy in Patients With Fabry Disease

Author

Onoue, Kenji, primary, Takemura, Genzou, additional, Nakano, Tomoya, additional, Miyazaki, Nagisa, additional, Tsujimoto, Akiko, additional, Watanabe, Takatomo, additional, Okada, Hideshi, additional, Kanamori, Hiromitsu, additional, Sugiura, Junichi, additional, Kanaoka, Koshiro, additional, Ishihara, Satomi, additional, Horii, Manabu, additional, Akai, Yasuhiro, additional, Sakaguchi, Yasuhiro, additional, and Saito, Yoshihiko, additional

Published
2019
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21. Factors Enhancing Serum Syndecan-1 Concentrations: A Large-Scale Comprehensive Medical Examination

Author

Oda, Kazumasa, primary, Okada, Hideshi, additional, Suzuki, Akio, additional, Tomita, Hiroyuki, additional, Kobayashi, Ryo, additional, Sumi, Kazuyuki, additional, Suzuki, Kodai, additional, Takada, Chihiro, additional, Ishihara, Takuma, additional, Suzuki, Keiko, additional, Kano, Soichiro, additional, Kondo, Kohei, additional, Iwashita, Yuki, additional, Yano, Hirohisa, additional, Zaikokuji, Ryogen, additional, Sampei, So, additional, Fukuta, Tetsuya, additional, Kitagawa, Yuichiro, additional, Okamoto, Haruka, additional, Watanabe, Takatomo, additional, Kawaguchi, Tomonori, additional, Kojima, Takao, additional, Deguchi, Fumiko, additional, Miyazaki, Nagisa, additional, Yamada, Noriaki, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Ushikoshi, Hiroaki, additional, Yoshida, Shozo, additional, Takemura, Genzou, additional, and Ogura, Shinji, additional

Published
2019
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22. Efficacy of Acupuncture Treatment for Improving the Respiratory Status in Patients Receiving Prolonged Mechanical Ventilation in Intensive Care Units: A Retrospective Observational Study

Author

Matsumoto-Miyazaki, Jun, primary, Ushikoshi, Hiroaki, additional, Suzuki, Kodai, additional, Miyazaki, Nagisa, additional, Nawa, Takahide, additional, Okada, Hideshi, additional, Yoshida, Shozo, additional, Murata, Ichijiro, additional, Ogura, Shinji, additional, and Minatoguchi, Shinya, additional

Published
2018
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23. Ultrastructural Alteration of Pulmonary Capillary Endothelial Glycocalyx During Endotoxemia

Author

Inagawa, Risa, primary, Okada, Hideshi, additional, Takemura, Genzou, additional, Suzuki, Kodai, additional, Takada, Chihiro, additional, Yano, Hirohisa, additional, Ando, Yoshiaki, additional, Usui, Takahiro, additional, Hotta, Yasuaki, additional, Miyazaki, Nagisa, additional, Tsujimoto, Akiko, additional, Zaikokuji, Ryogen, additional, Matsumoto, Atsumu, additional, Kawaguchi, Tomonori, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Yoshida, Shozo, additional, Kumada, Keisuke, additional, Ushikoshi, Hiroaki, additional, Toyoda, Izumi, additional, and Ogura, Shinji, additional

Published
2018
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24. Mitochondrial deformity confined to a single cardiomyocyte in human endomyocardial biopsy specimens: Report of 4 cases

Author

Takemura, Genzou, primary, Kanamori, Hiromitsu, additional, Okada, Hideshi, additional, Tsujimoto, Akiko, additional, Miyazaki, Nagisa, additional, Miyata, Shusaku, additional, Ohta, Hideaki, additional, Kawase, Yoshiaki, additional, Ono, Makoto, additional, Mochizuki, Mamoru, additional, Kobayashi, Shigeki, additional, Onoue, Kenji, additional, Nakano, Tomoya, additional, Sakaguchi, Yasuhiro, additional, Matsuo, Hitoshi, additional, Yano, Masafumi, additional, and Saito, Yoshihiko, additional

Published
2017
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25. Three-dimensional ultrastructure of capillary endothelial glycocalyx under normal and experimental endotoxemic conditions

Author

Okada, Hideshi, primary, Takemura, Genzou, additional, Suzuki, Kodai, additional, Oda, Kazumasa, additional, Takada, Chihiro, additional, Hotta, Yasuaki, additional, Miyazaki, Nagisa, additional, Tsujimoto, Akiko, additional, Muraki, Isamu, additional, Ando, Yoshiaki, additional, Zaikokuji, Ryogen, additional, Matsumoto, Atsumu, additional, Kitagaki, Hiroki, additional, Tamaoki, Yuto, additional, Usui, Takahiro, additional, Doi, Tomoaki, additional, Yoshida, Takahiro, additional, Yoshida, Shozo, additional, Ushikoshi, Hiroaki, additional, Toyoda, Izumi, additional, and Ogura, Shinji, additional

Published
2017
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27. Possible mechanism for disposal of degenerative cardiomyocytes in human failing hearts: phagocytosis by a neighbour.

Author

Takemura, Genzou, Onoue, Kenji, Nakano, Tomoya, Nakamura, Takuya, Sakaguchi, Yasuhiro, Tsujimoto, Akiko, Miyazaki, Nagisa, Watanabe, Takatomo, Kanamori, Hiromitsu, Okada, Hideshi, Kawasaki, Masanori, Fujiwara, Takako, Fujiwara, Hisayoshi, and Saito, Yoshihiko

Subjects
HEART cells, DILATED cardiomyopathy, PHAGOCYTOSIS
Abstract

The index case was a 51‐year‐old woman suffering from doxorubicin cardiomyopathy. In her endomyocardial biopsy specimen, we observed under electron microscopy six scenes in which degenerative cardiomyocytes were engulfed by neighbouring cardiomyocytes. The enclosed cardiomyocytes appeared more degenerative than the enclosing ones in every pair: the myofibrils were more severely damaged. At more degenerative stages, some desmosomes of the intercalated discs on the enclosed cardiomyocyte had disappeared. The membranes between the cardiomyocytes were occasionally disrupted, and there appeared to be sharing of cellular contents between the cells. One pair of such a phagocytosis‐like figure was observed in one case with 5‐fluorouracil cardiomyopathy (a 68‐year‐old man) among eight other chemotherapy‐induced cardiomyopathies but none among 30 non‐drug‐induced dilated cardiomyopathies. The findings suggest a mechanism for disposal of degenerative cardiomyocytes in human failing hearts: phagocytosis by a neighbour, although alternative interpretations remain (e.g. giant autophagic vacuoles or two cardiomyocytes with degenerative intercalated discs). [ABSTRACT FROM AUTHOR]

Published
2019
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31. Intravenous Administration of Endothelial Colony-Forming Cells Overexpressing Integrin β1 Augments Angiogenesis in Ischemic Legs

Author

Goto, Kazuko, primary, Takemura, Genzou, additional, Takahashi, Tomoyuki, additional, Okada, Hideshi, additional, Kanamori, Hiromitsu, additional, Kawamura, Itta, additional, Watanabe, Takatomo, additional, Morishita, Kentaro, additional, Tsujimoto, Akiko, additional, Miyazaki, Nagisa, additional, Ushikoshi, Hiroaki, additional, Kawasaki, Masanori, additional, Mikami, Atsushi, additional, Kosai, Ken-ichiro, additional, and Minatoguchi, Shinya, additional

Published
2015
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34. Phenotype and Physiological Significance of the Endocardial Smooth Muscle Cells in Human Failing Hearts

Author

Okada, Hideshi, primary, Takemura, Genzou, additional, Kanamori, Hiromitsu, additional, Tsujimoto, Akiko, additional, Goto, Kazuko, additional, Kawamura, Itta, additional, Watanabe, Takatomo, additional, Morishita, Kentaro, additional, Miyazaki, Nagisa, additional, Tanaka, Toshiki, additional, Ushikoshi, Hiroaki, additional, Kawasaki, Masanori, additional, Miyazaki, Tatsuhiko, additional, Suzui, Natsuko, additional, Nishigaki, Kazuhiko, additional, Mikami, Atsushi, additional, Ogura, Shinji, additional, and Minatoguchi, Shinya, additional

Published
2015
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35. Blood purification therapy for acute hepatic failure caused by Amanita virosa

Author

Yoshida, Shozo, primary, Okada, Hideshi, additional, Doi, Tomoaki, additional, Nakajima, Yasuhiro, additional, Suzuki, Kodai, additional, Tanaka, Taku, additional, Fukuta, Tetsuya, additional, Kitagawa, Yuichiro, additional, Yasuda, Ryu, additional, Mizuno, Yosuke, additional, Miyazaki, Nagisa, additional, Morishita, Kentaro, additional, Ushikoshi, Hiroaki, additional, Takemura, Genzou, additional, Shirai, Kunihiro, additional, Toyoda, Izumi, additional, and Ogura, Shinji, additional

Published
2015
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37. Ultrastructural alteration of pulmonary tissue under conditions of high oxygen concentration.

Author

Yano H, Kuroda A, Okada H, Tomita H, Suzuki K, Takada C, Fukuda H, Kawasaki Y, Muraki I, Wakayama Y, Kano S, Tamaoki Y, Nishio A, Inagawa R, Sampei S, Kamidani R, Kakino Y, Yasuda R, Kitagawa Y, Fukuta T, Miyake T, Kanda N, Miyazaki N, Doi T, Yoshida T, Suzuki A, Yoshida S, and Ogura S

Abstract

Objective: To determine the structure of pulmonary tissue under conditions of high oxygen concentration., Methods: Ten-week-old C57BL male mice and control mice were exposed to 100% oxygen and to room air for 72 hours, respectively. To follow the progression of lesions, the mice were sacrificed at 6, 12, 24, 48, and 72 hours after 100% oxygen administration. Lung specimens obtained from these mice underwent morphologic analysis and immunofluorescence studies. We used scanning and transmission electron microscopy to determine the ultrastructure of the pulmonary capillaries, including the endothelial glycocalyx. To visualize the endothelial glycocalyx, we performed lanthanum nitrate staining., Results: The survival rate of the 100% oxygen administration group was 5% (2/40) and that of the control group was 100%. Perivascular cavity enlargement was detected 12 hours after 100% oxygen administration and expanded over time. Ultrastructural analysis using electron microscopy revealed collapsed alveoli and pulmonary capillary wall and alveolar wall thickening in the 100% oxygen group. The pulmonary capillary endothelial glycocalyx was injured in the 100% oxygen group. The perivascular cavity decreased in mice that were returned to room air after 48 hours of 100% oxygen administration., Conclusion: High-concentration oxygen causes perivascular cavity enlargement; this is thought to be a special characteristic of high oxygen damage. In addition, high-concentration oxygen may be involved in pulmonary endothelial glycocalyx injury., Competing Interests: None., (IJCEP Copyright © 2020.)

Published
2020

38. Tenascin-C expression in renal biopsies from patients with tubulointerstitial nephritis and its relation to disease activity and prognosis.

Author

Izumi K, Miyazaki N, Okada H, Tsujimoto A, Matsumoto-Miyazaki J, Naito J, Yoshida G, Murata I, Nagashima K, Ohno M, Imanaka-Yoshida K, Okura H, Ohashi H, and Takemura G

Abstract

Tenascin-C (TNC) is an extracellular matrix protein that is transiently expressed in close association with tissue remodeling in various organs. Expression of TNC in patients with tubulointerstitial nephritis (TIN) is not well-characterized. Using renal biopsy specimens from 25 patients with TIN and 8 patients with thin basement membrane disease (controls), we assessed immunohistochemical staining for TNC and investigated its relation with clinicopathologic data. TNC was undetectable in the controls, but TNC was observed in the interstitium of specimens from all patients with TIN, and strong TNC staining was detected within active tubulitis lesions. TNC was not principally expressed in glomeruli, and it was also absent from scar tissue. Comparison with Sirius red staining revealed that TNC was present where collagen fibers had not yet formed. The percent area of TNC within the interstitium (% TNC-positive area) showed a significant negative correlation with illness duration and significant positive correlations with the serum CRP level and eGFR aggravation, both of which reflect disease activity. On the other hand, no correlation was found between % TNC-positive area and eGFR recovery during 2 years of follow up. Examination of renal biopsy specimens from TIN patients revealed that TNC appears during the active stage of inflammation and then disappears with healing. This suggests that TNC expression reflects TIN disease activity, but not prognosis., Competing Interests: None., (IJCEP Copyright © 2020.)

Published
2020

39. Vacuolated cardiomyocytes in human endomyocardial biopsy specimens.

Author

Takemura G, Onoue K, Arimoto T, Watanabe T, Tsujimoto A, Takada C, Okada H, Nakano T, Sakaguchi Y, Miyazaki N, Watanabe T, Kanamori H, Ogura S, Saito Y, Fujiwara T, Fujiwara H, and Hotta Y

Abstract

We encountered an unfamiliar finding during electron microscopic examination of an endomyocardial biopsy obtained from a 55-year-old woman suffering from heart failure due to dilated phase hypertrophic cardiomyopathy. Many cardiomyocytes contained large vacuoles that were mainly empty except for small amounts of amorphous substrate. These were not autophagic vacuoles, as they lacked limiting membranes. Six years later, we encountered similar histological findings in three successive biopsies sourced from another hospital. They were obtained from a 77-year-old man with hypertrophic cardiomyopathy, a 28-year-old woman with endocardial fibrosis, and a 33-year-old man with dilated cardiomyopathy. This biopsy was the second for the endocardial fibrosis patient, and her first biopsy showed no vacuoles within cardiomyocytes. Close inspection of the procedures revealed that in all of these cases the fixed biopsy specimens were carried to the hospital from other institutes using a refrigerated courier service. We then fixed rat heart tissues, froze them once, and processed them for electron microscopy. In that experiment, we were able to reproduce the vacuolar cardiomyocytes, thereby demonstrating it to be a laboratory artifact. We therefore want to emphasize to physicians not to freeze biopsy specimens and not to use a refrigerated courier service for their transport. < Learning objective: Under an electron microscope, large vacuoles were observed within many cardiomyocytes in endomyocardial biopsies obtained from 4 patients with cardiomyopathies of different etiologies, which were not autophagic vacuoles. Since an animal experiment could reproduce a similar histological finding by freezing the tissue after fixation, such an unfamiliar finding was considered to be a laboratory artifact. We would call physicians' attention not to freeze the biopsy specimens even after fixation.>., (© 2019 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

Published
2019
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40. Intravenous Administration of Endothelial Colony-Forming Cells Overexpressing Integrin β1 Augments Angiogenesis in Ischemic Legs.

Author

Goto K, Takemura G, Takahashi T, Okada H, Kanamori H, Kawamura I, Watanabe T, Morishita K, Tsujimoto A, Miyazaki N, Ushikoshi H, Kawasaki M, Mikami A, Kosai K, and Minatoguchi S

Subjects
Animals, Endothelial Progenitor Cells cytology, Endothelial Progenitor Cells metabolism, Femoral Artery surgery, Fibronectins genetics, Fibronectins metabolism, Gene Expression Regulation, Genes, Reporter, Genetic Vectors, Green Fluorescent Proteins genetics, Green Fluorescent Proteins metabolism, Hindlimb metabolism, Hindlimb pathology, Humans, Injections, Intravenous, Integrin beta1 metabolism, Ischemia genetics, Ischemia metabolism, Ischemia pathology, Lentivirus genetics, Ligation, Male, Mice, Mice, Inbred NOD, Mice, SCID, Transduction, Genetic, Transgenes, Transplantation, Heterologous, Endothelial Progenitor Cells transplantation, Fibronectins agonists, Hindlimb blood supply, Integrin beta1 genetics, Ischemia therapy, Neovascularization, Physiologic
Abstract

When injected directly into ischemic tissue in patients with peripheral artery disease, the reparative capacity of endothelial progenitor cells (EPCs) appears to be limited by their poor survival. We, therefore, attempted to improve the survival of transplanted EPCs through intravenous injection and gene modification. We anticipated that overexpression of integrin β1 will enable injected EPCs to home to ischemic tissue, which abundantly express extracellular matrix proteins, the ligands for integrins. In addition, integrin β1 has an independent angiogenesis-stimulating function. Human endothelial colony-forming cells (ECFCs; late-outgrowth EPCs) were transduced using a lentiviral vector encoding integrin β1 (ITGB1) or enhanced green fluorescent protein (GFP). We then locally or systemically injected phosphate-buffered saline or the genetically modified ECFCs (GFP-ECFCs or ITGB1-ECFCs; 1 × 10(5) cells each) into NOD/Shi-scid, IL-2Rγnull mice whose right femoral arteries had been occluded 24 hours earlier. Upregulation of extracellular matrix proteins, including fibronectin, was apparent in the ischemic legs. Four weeks later, blood perfusion of the ischemic limb was significantly augmented only in the ITGB1-ECFC group. Scanning electron microscopy of vascular casts revealed increases in the perfused blood vessels in the ischemic legs of mice in the ITGB1-ECFC group and significant increases in the density of both capillaries and arterioles. Transplanted ECFC-derived vessels accounted for 28% ± 4.2% of the vessels in the ITGB1-ECFC group, with no cell fusion. Intravenous administration of ECFCs engineered to home to ischemic tissue appears to efficiently mediate therapeutic angiogenesis in a mouse model of peripheral artery disease. Significance: The intravenous administration of endothelial colony-forming cells (ECFCs) genetically modified to overexpress integrin β1 effectively stimulated angiogenesis in ischemic mouse hindlimbs. Transplanted ECFCs were observed in the ischemic leg tissue, even at the chronic stage. Moreover, the cells appeared functional, as evidenced by the improved blood flow. The cell type used (ECFCs), the route of administration (intravenous, not directly injected into the affected area), and the use of ligand-receptor interactions (extracellular matrix and integrins) for homing represent substantial advantages over previously reported cell therapies for the treatment of peripheral artery disease., (©AlphaMed Press.)

Published
2016
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41. Expression of prorenin receptor in renal biopsies from patients with IgA nephropathy.

Author

Miyazaki N, Murata I, Takemura G, Okada H, Kanamori H, Matsumoto-Miyazaki J, Yoshida G, Izumi K, Kashi H, Niimi K, Nishiwaki A, Miyazaki T, Ohno M, Ohashi H, Suzuki F, and Minatoguchi S

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Biopsy, Disease Progression, Female, Fibrosis, Glomerulonephritis, IGA pathology, Glomerulonephritis, IGA surgery, Humans, Immunohistochemistry, Kidney metabolism, Kidney pathology, Kidney Diseases pathology, Kidney Diseases surgery, Male, Microscopy, Immunoelectron, Middle Aged, Nephrectomy, Young Adult, Glomerulonephritis, IGA metabolism, Kidney Diseases metabolism, Microtubule-Associated Proteins metabolism, Receptors, Cell Surface metabolism, Vacuolar Proton-Translocating ATPases metabolism
Abstract

Prorenin receptor (PRR) has been implicated in the onset and progression of various renal diseases, though its possible association with immunoglobulin A (IgA) nephropathy remains unclear. In the present study, we tried to clarify expression and pathophysiological significance of PRR in IgA nephropathy. We immunohistochemically assessed PRR levels in renal biopsy specimens from 48 patients with IgA nephropathy and evaluated its relevance to the clinical and pathological features of the disease. PRR was detected mainly in renal tubular cells, which was confirmed at the subcellular level using immunoelectron microscopy. The PRR-positive area (%PRR area) correlated with daily urinary protein, which is known to reflect disease severity (r=0.286, P=0.049). PRR levels were weaker in tubular cells bordering areas of severe interstitial fibrosis, where α-smooth muscle actin-positive myofibroblasts were present. We also used immunohistochemical detection of microtubule-associated protein-1 light chain 3 (LC3) and electron microscopy to assess autophagy, a cytoprotective mechanism downstream of PRR. We noted an apparent coincidence between autophagy activation in tubular cells and PRR expression in the same cells. Taken together, our findings suggest that renal expression of PRR in IgA nephropathy may be a compensatory response slowing disease progression by preventing tubular cell death and subsequent fibrosis through activation of cytoprotective autophagic machinery. Further studies using different type of kidney diseases could draw conclusion if the present finding is a generalized observation beyond IgA nephropathy.

Published
2014

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