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2. Impaired Relaxation in Induced Pluripotent Stem Cell‐Derived Cardiomyocytes with Pathogenic TNNI3 Mutation of Pediatric Restrictive Cardiomyopathy

Author

Wang, Renjie, primary, Hasegawa, Moyu, additional, Suginobe, Hidehiro, additional, Yoshihara, Chika, additional, Ishii, Yoichiro, additional, Ueyama, Atsuko, additional, Ueda, Kazutoshi, additional, Hashimoto, Kazuhisa, additional, Hirose, Masaki, additional, Ishii, Ryo, additional, Narita, Jun, additional, Watanabe, Takuji, additional, Kawamura, Takuji, additional, Taira, Masaki, additional, Ueno, Takayoshi, additional, Miyagawa, Shigeru, additional, and Ishida, Hidekazu, additional

Published
2024
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4. GFRA2 Identifies Cardiac Progenitors and Mediates Cardiomyocyte Differentiation in a RET-Independent Signaling Pathway

Author

Ishida, Hidekazu, primary, Saba, Rie, additional, Kokkinopoulos, Ioannis, additional, Hashimoto, Masakazu, additional, Yamaguchi, Osamu, additional, Nowotschin, Sonja, additional, Shiraishi, Manabu, additional, Ruchaya, Prashant, additional, Miller, Duncan, additional, Harmer, Stephen, additional, Poliandri, Ariel, additional, Kogaki, Shigetoyo, additional, Sakata, Yasushi, additional, Dunkel, Leo, additional, Tinker, Andrew, additional, Hadjantonakis, Anna-Katerina, additional, Sawa, Yoshiki, additional, Sasaki, Hiroshi, additional, Ozono, Keiichi, additional, Suzuki, Ken, additional, and Yashiro, Kenta, additional

Published
2023
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6. Isogenic pairs of induced-pluripotent stem-derived endothelial cells identify DYRK1A/PPARG/EGR1 pathway is responsible for Down syndrome-associated pulmonary hypertension

Author

Suginobe, Hidehiro, primary, Ishida, Hidekazu, additional, Ishii, Yoichiro, additional, Ueda, Kazutoshi, additional, Yoshihara, Chika, additional, Ueyama, Atsuko, additional, Wang, Renjie, additional, Tsuru, Hirofumi, additional, Hashimoto, Kazuhisa, additional, Hirose, Masaki, additional, Ishii, Ryo, additional, Narita, Jun, additional, Kitabatake, Yasuji, additional, and Ozono, Keiichi, additional

Published
2023
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7. Use of the index of pulmonary vascular disease for predicting long-term outcome of pulmonary arterial hypertension associated with congenital heart disease

Author

Chida-Nagai, Ayako, primary, Masaki, Naoki, additional, Maeda, Kay, additional, Sasaki, Konosuke, additional, Sato, Hiroki, additional, Muneuchi, Jun, additional, Ochiai, Yoshie, additional, Murayama, Hiroomi, additional, Tahara, Masahiro, additional, Shiono, Atsuko, additional, Shinozuka, Atsushi, additional, Kono, Fumihiko, additional, Machida, Daisuke, additional, Toyooka, Shinichi, additional, Sugimoto, Seiichiro, additional, Nakamura, Kazufumi, additional, Akagi, Satoshi, additional, Kondo, Maiko, additional, Kasahara, Shingo, additional, Kotani, Yasuhiro, additional, Koizumi, Junichi, additional, Oda, Katsuhiko, additional, Harada, Masako, additional, Nakajima, Daisuke, additional, Murata, Akira, additional, Nagata, Hazumu, additional, Yatsunami, Koichi, additional, Kobayashi, Tomio, additional, Matsunaga, Yoshikiyo, additional, Inoue, Takahiro, additional, Yamagishi, Hiroyuki, additional, Nakagawa, Naomi, additional, Ohtani, Katsuki, additional, Yamamoto, Masaki, additional, Ito, Yushi, additional, Hokosaki, Tatsunori, additional, Kuwahara, Yuta, additional, Masutani, Satoshi, additional, Nomura, Koji, additional, Wada, Tsutomu, additional, Sawada, Hirofumi, additional, Abiko, Masayuki, additional, Takahashi, Tatsunori, additional, Ishikawa, Yuichi, additional, Okada, Seigo, additional, Naitoh, Atsushi, additional, Toda, Takako, additional, Ando, Tatsuya, additional, Masuzawa, Akihiro, additional, Hoshino, Shinsuke, additional, Kawada, Masaaki, additional, Nomura, Yuichi, additional, Ueno, Kentaro, additional, Ohashi, Naoki, additional, Tachibana, Tsuyoshi, additional, Cao, Yuchen, additional, Ueda, Hideaki, additional, Yanagi, Sadamitsu, additional, Koide, Masaaki, additional, Mitsushita, Norie, additional, Higashi, Kouji, additional, Minosaki, Yoshihiro, additional, Hayashi, Tomohiro, additional, Okamoto, Takashi, additional, Kuraishi, Kenji, additional, Ehara, Eiji, additional, Ishida, Hidekazu, additional, Horigome, Hitoshi, additional, Murakami, Takashi, additional, Takei, Kohta, additional, Ishii, Taku, additional, Harada, Gen, additional, Hirata, Yasutaka, additional, Maeda, Jun, additional, Tatebe, Shunsuke, additional, Ota, Chiharu, additional, Hayabuchi, Yasunobu, additional, Sakazaki, Hisanori, additional, Sasaki, Takashi, additional, Hirono, Keiichi, additional, Suzuki, Sayo, additional, Yasuda, Masahiro, additional, Takeda, Atsuhito, additional, Sawai, Madoka, additional, Miyaji, Kagami, additional, Kitagawa, Atsushi, additional, Nakai, Yosuke, additional, Kakimoto, Nobuyuki, additional, Agematsu, Kouta, additional, Manabe, Atsushi, additional, and Saiki, Yoshikatsu, additional

Published
2023
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9. Clinical Outcomes and Genetic Analyses of Restrictive Cardiomyopathy in Children

Author

Ishida, Hidekazu, primary, Narita, Jun, additional, Ishii, Ryo, additional, Suginobe, Hidehiro, additional, Tsuru, Hirofumi, additional, Wang, Renjie, additional, Yoshihara, Chika, additional, Ueyama, Atsuko, additional, Ueda, Kazutoshi, additional, Hirose, Masaki, additional, Hashimoto, Kazuhisa, additional, Nagano, Hiroki, additional, Kogaki, Shigetoyo, additional, Kuramoto, Yuki, additional, Miyashita, Yohei, additional, Asano, Yoshihiro, additional, and Ozono, Keiichi, additional

Published
2023
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11. Pathogenic Roles of Cardiac Fibroblasts in Pediatric Dilated Cardiomyopathy

Author

Tsuru, Hirofumi, primary, Yoshihara, Chika, additional, Suginobe, Hidehiro, additional, Matsumoto, Mizuki, additional, Ishii, Yoichiro, additional, Narita, Jun, additional, Ishii, Ryo, additional, Wang, Renjie, additional, Ueyama, Atsuko, additional, Ueda, Kazutoshi, additional, Hirose, Masaki, additional, Hashimoto, Kazuhisa, additional, Nagano, Hiroki, additional, Tanaka, Ryosuke, additional, Okajima, Takaharu, additional, Ozono, Keiichi, additional, and Ishida, Hidekazu, additional

Published
2023
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13. Clinical Outcomes and Genetic Analyses of Restrictive Cardiomyopathy in Children

Author

1000050467552, Ishida, Hidekazu, 1000070467562, Narita, Jun, 1000090794008, Ishii, Ryo, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, Yoshihara, Chika, Ueyama, Atsuko, Ueda, Kazutoshi, 1000010973662, Hirose, Masaki, Hashimoto, Kazuhisa, Nagano, Hiroki, Kogaki, Shigetoyo, 1000050843794, Kuramoto, Yuki, 1000060816312, 0000-0002-1739-4734, Miyashita, Yohei, 1000060527670, Asano, Yoshihiro, 1000020270770, Ozono, Keiichi, 1000050467552, Ishida, Hidekazu, 1000070467562, Narita, Jun, 1000090794008, Ishii, Ryo, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, Yoshihara, Chika, Ueyama, Atsuko, Ueda, Kazutoshi, 1000010973662, Hirose, Masaki, Hashimoto, Kazuhisa, Nagano, Hiroki, Kogaki, Shigetoyo, 1000050843794, Kuramoto, Yuki, 1000060816312, 0000-0002-1739-4734, Miyashita, Yohei, 1000060527670, Asano, Yoshihiro, 1000020270770, and Ozono, Keiichi

Abstract

Ishida H., Narita J., Ishii R., et al. Clinical Outcomes and Genetic Analyses of Restrictive Cardiomyopathy in Children. Circulation: Genomic and Precision Medicine 16, 382 (2023); https://doi.org/10.1161/CIRCGEN.122.004054., BACKGROUND: Restrictive cardiomyopathy in children is rare and outcomes are very poor. However, little information is available concerning genotype-outcome correlations. METHODS: We analyzed the clinical characteristics and genetic testing, including whole exome sequencing, of 28 pediatric restrictive cardiomyopathy patients who were diagnosed from 1998 to 2021 at Osaka University Hospital in Japan. RESULTS: The median age at diagnosis (interquartile range) was 6 (2.25-8.5) years. Eighteen patients received heart transplantations and 5 patients were on the waiting list. One patient died while waiting for transplantation. Pathologic or likely-pathogenic variants were identified in 14 of the 28 (50%) patients, including heterozygous TNNI3 missense variants in 8 patients. TNNT2, MYL2, and FLNC missense variants were also identified. No significant differences in clinical manifestations and hemodynamic parameters between positive and negative pathogenic variants were detected. However, 2- and 5-year survival rates were significantly lower in patients with pathogenic variants (50% and 22%) compared with survival in patients without pathogenic variants (62% and 54%; P=0.0496, log-rank test). No significant differences were detected in the ratio of patients diagnosed at nationwide school heart disease screening program between positive and negative pathogenic variants. Patients diagnosed by school screening showed better transplant-free survival compared with patients diagnosed by heart failure symptoms (P=0.0027 in log-rank test). CONCLUSIONS: In this study, 50% of pediatric restrictive cardiomyopathy patients had pathogenic or likely-pathogenic gene variants, and TNNI3 missense variants were the most frequent. Patients with pathogenic variants showed significantly lower transplant-free survival compared with patients without pathogenic variants.

Published
2023

17. Atomic force microscopy identifies the alteration of rheological properties of the cardiac fibroblasts in idiopathic restrictive cardiomyopathy

Author

Matsumoto, Mizuki, primary, Tsuru, Hirofumi, additional, Suginobe, Hidehiro, additional, Narita, Jun, additional, Ishii, Ryo, additional, Hirose, Masaki, additional, Hashimoto, Kazuhisa, additional, Wang, Renjie, additional, Yoshihara, Chika, additional, Ueyama, Atsuko, additional, Tanaka, Ryosuke, additional, Ozono, Keiichi, additional, Okajima, Takaharu, additional, and Ishida, Hidekazu, additional

Published
2022
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18. Alternatively activated macrophages determine repair of the infarcted adult murine heart

Author

Shiraishi, Manabu, Shintani, Yasunori, Shintani, Yusuke, Ishida, Hidekazu, Saba, Rie, Yamaguchi, Atsushi, Adachi, Hideo, Yashiro, Kenta, and Suzuki, Ken

Subjects
Heart attack -- Care and treatment, Biological products -- Innovations, Phosphotransferases -- Health aspects, Macrophages -- Genetic aspects, Health care industry
Abstract

Alternatively activated (also known as M2) macrophages are involved in the repair of various types of organs. However, the contribution of M2 macrophages to cardiac repair after myocardial infarction (MI) remains to be fully characterized. Here, we identified [CD206.sup.+]F4/[80.sup.+][CD11b.sup.+] M2-like macrophages in the murine heart and demonstrated that this cell population predominantly increases in the infarct area and exhibits strengthened reparative abilities after MI. We evaluated mice lacking the kinase TRIB1 ([Trib1.sup.-/-]), which exhibit a selective depletion of M2 macrophages after MI. Compared with control animals, [Trib1.sup.-/-] mice had a catastrophic prognosis, with frequent cardiac rupture, as the result of markedly reduced collagen fibril formation in the infarct area due to impaired fibroblast activation. The decreased tissue repair observed in [Tribl.sup.-/-] mice was entirely rescued by an external supply of M2-like macrophages. Furthermore, IL-1α and osteopontin were suggested to be mediators of M2-like macrophage-induced fibroblast activation. In addition, IL-4 administration achieved a targeted increase in the number of M2-like macrophages and enhanced the post-MI prognosis of WT mice, corresponding with amplified fibroblast activation and formation of more supportive fibrous tissues in the infarcts. Together, these data demonstrate that M2-like macrophages critically determine the repair of infarcted adult murine heart by regulating fibroblast activation and suggest that IL-4 is a potential biological drug for treating MI., Introduction The formation of connective tissue is an essential process in the healing and repair of almost every tissue and organ, and this process is of particular importance in the [...]

Published
2016
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19. Riociguat in children with pulmonary arterial hypertension: The PATENT–CHILD study

Author

García Aguilar, Humberto, primary, Gorenflo, Matthias, additional, Ivy, D. Dunbar, additional, Moledina, Shahin, additional, Castaldi, Biagio, additional, Ishida, Hidekazu, additional, Cześniewicz, Paweł, additional, Kusa, Jacek, additional, Miera, Oliver, additional, Pattathu, Joseph, additional, Weng, Ken‐Pen, additional, Ablonczy, Laszlo, additional, Apitz, Christian, additional, Katona, Marta, additional, Kurosaki, Kenichi, additional, Pulido, Tomas, additional, Yamagishi, Hiroyuki, additional, Yasuda, Kazushi, additional, Cisternas, Galia, additional, Goth, Melanie, additional, Lippert, Susanne, additional, Radomskyj, Anna, additional, Saleh, Soundos, additional, Willmann, Stefan, additional, Wirsching, Gabriela, additional, Bonnet, Damien, additional, and Beghetti, Maurice, additional

Published
2022
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21. Atomic force microscopy identifies the alteration of rheological properties of the cardiac fibroblasts in idiopathic restrictive cardiomyopathy

Author

Matsumoto, Mizuki, Tsuru, Hirofumi, Suginobe, Hidehiro, Narita, Jun, Ishii, Ryo, Hirose, Masaki, Hashimoto, Kazuhisa, Wang, Renjie, Yoshihara, Chika, Ueyama, Atsuko, Tanaka, Ryosuke, Ozono, Keiichi, Okajima, Takaharu, Ishida, Hidekazu, Matsumoto, Mizuki, Tsuru, Hirofumi, Suginobe, Hidehiro, Narita, Jun, Ishii, Ryo, Hirose, Masaki, Hashimoto, Kazuhisa, Wang, Renjie, Yoshihara, Chika, Ueyama, Atsuko, Tanaka, Ryosuke, Ozono, Keiichi, Okajima, Takaharu, and Ishida, Hidekazu

Abstract

Restrictive cardiomyopathy (RCM) is a rare disease characterized by increased ventricular stiffness and preserved ventricular contraction. Various sarcomere gene variants are known to cause RCM; however, more than a half of patients do not harbor such pathogenic variants. We recently demonstrated that cardiac fibroblasts (CFs) play important roles in inhibiting the diastolic function of cardiomyocytes via humoral factors and direct cell-cell contact regardless of sarcomere gene mutations. However, the mechanical properties of CFs that are crucial for intercellular communication and the cardiomyocyte microenvironment remain less understood. In this study, we evaluated the rheological properties of CFs derived from pediatric patients with RCM and healthy control CFs via atomic force microscopy. Then, we estimated the cellular modulus scale factor related to the cell stiffness, fluidity, and Newtonian viscosity of single cells based on the single power-law rheology model and analyzed the comprehensive gene expression profiles via RNA-sequencing. RCM-derived CFs showed significantly higher stiffness and viscosity and lower fluidity compared to healthy control CFs. Furthermore, RNA-sequencing revealed that the signaling pathways associated with cytoskeleton elements were affected in RCM CFs; specifically, cytoskeletal actin-associated genes (ACTN1, ACTA2, and PALLD) were highly expressed in RCM CFs, whereas several tubulin genes (TUBB3, TUBB, TUBA1C, and TUBA1B) were down-regulated. These results implies that the signaling pathways associated with cytoskeletal elements alter the rheological properties of RCM CFs, particularly those related to CF-cardiomyocyte interactions, thereby leading to diastolic cardiac dysfunction in RCM.

Published
2022

23. Pharmacological Alteration of Cellular Mechanical Properties in Pulmonary Arterial Smooth Muscle Cells of Idiopathic Pulmonary Arterial Hypertension

Author

Katsuragi, Shinichi, primary, Tatsumi, Nao, additional, Matsumoto, Mizuki, additional, Narita, Jun, additional, Ishii, Ryo, additional, Suginobe, Hidehiro, additional, Tsuru, Hirofumi, additional, Wang, Renjie, additional, Kogaki, Shigetoyo, additional, Tanaka, Ryosuke, additional, Ozono, Keiichi, additional, Okajima, Takaharu, additional, and Ishida, Hidekazu, additional

Published
2021
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24. Pharmacological Alteration of Cellular Mechanical Properties in Pulmonary Arterial Smooth Muscle Cells of Idiopathic Pulmonary Arterial Hypertension

Author

Katsuragi, Shinichi, Tatsumi, Nao, Matsumoto, Mizuki, Narita, Jun, Ishii, Ryo, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, Kogaki, Shigetoyo, Tanaka, Ryosuke, Ozono, Keiichi, Okajima, Takaharu, Ishida, Hidekazu, Katsuragi, Shinichi, Tatsumi, Nao, Matsumoto, Mizuki, Narita, Jun, Ishii, Ryo, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, Kogaki, Shigetoyo, Tanaka, Ryosuke, Ozono, Keiichi, Okajima, Takaharu, and Ishida, Hidekazu

Abstract

Background: Idiopathic pulmonary arterial hypertension (IPAH) is a progressive disease caused by vascular remodeling of the pulmonary arteries with elevated pulmonary vascular resistance. Recently, various pulmonary vasodilator drugs have become available in the clinical field, and have dramatically ameliorated the prognosis of IPAH. However, little is known about how the mechanical properties of pulmonary arterial smooth muscle cells (PASMCs) are altered under drug supplementation. Methods: Atomic force microscopy (AFM) was used to investigate the mechanical properties of PASMCs derived from a patient with IPAH (PAH-PASMCs) and a healthy control (N-PASMCs) which received the supplementation of clinically used drugs for IPAH: sildenafil, macitentan, and riociguat. Results: PASMCs derived from PAH-PASMCs were stiffer than those derived from N-PASMCs. With sildenafil treatment, the apparent Young's modulus (E-0) of cells significantly decreased in PAH-PASMCs but remained unchanged in N-PASMCs. The decrease in E-0 of PAH-PASMCs was also observed in macitentan and riociguat treatment. The stress relaxation AFM revealed that the decrease in E-0 of PAH-PASMCs resulted from a decrease in the cell elastic modulus and/or increase in cell fluidity. The combination treatment of macitentan and riociguat showed an additive effect on cell mechanical properties, implying that this clinically accepted combination therapy for IPAH influences the intracellular mechanical components. Conclusions: Pulmonary vasodilator drugs affect the mechanical properties of PAH-PASMCs, and there exists a mechanical effect of combination treatment on PAH-PASMCs.

Published
2021

25. Pharmacological Alteration of Cellular Mechanical Properties in Pulmonary Arterial Smooth Muscle Cells of Idiopathic Pulmonary Arterial Hypertension

Author

1000040774261, Katsuragi, Shinichi, Tatsumi, Nao, Matsumoto, Mizuki, 1000070467562, Narita, Jun, Ishii, Ryo, 1000030791595, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, 1000000311754, Kogaki, Shigetoyo, Tanaka, Ryosuke, 1000020270770, Ozono, Keiichi, 1000070280998, Okajima, Takaharu, 1000050467552, Ishida, Hidekazu, 1000040774261, Katsuragi, Shinichi, Tatsumi, Nao, Matsumoto, Mizuki, 1000070467562, Narita, Jun, Ishii, Ryo, 1000030791595, Suginobe, Hidehiro, Tsuru, Hirofumi, Wang, Renjie, 1000000311754, Kogaki, Shigetoyo, Tanaka, Ryosuke, 1000020270770, Ozono, Keiichi, 1000070280998, Okajima, Takaharu, 1000050467552, and Ishida, Hidekazu

Abstract

Background: Idiopathic pulmonary arterial hypertension (IPAH) is a progressive disease caused by vascular remodeling of the pulmonary arteries with elevated pulmonary vascular resistance. Recently, various pulmonary vasodilator drugs have become available in the clinical field, and have dramatically ameliorated the prognosis of IPAH. However, little is known about how the mechanical properties of pulmonary arterial smooth muscle cells (PASMCs) are altered under drug supplementation. Methods: Atomic force microscopy (AFM) was used to investigate the mechanical properties of PASMCs derived from a patient with IPAH (PAH-PASMCs) and a healthy control (N-PASMCs) which received the supplementation of clinically used drugs for IPAH: sildenafil, macitentan, and riociguat. Results: PASMCs derived from PAH-PASMCs were stiffer than those derived from N-PASMCs. With sildenafil treatment, the apparent Young's modulus (E-0) of cells significantly decreased in PAH-PASMCs but remained unchanged in N-PASMCs. The decrease in E-0 of PAH-PASMCs was also observed in macitentan and riociguat treatment. The stress relaxation AFM revealed that the decrease in E-0 of PAH-PASMCs resulted from a decrease in the cell elastic modulus and/or increase in cell fluidity. The combination treatment of macitentan and riociguat showed an additive effect on cell mechanical properties, implying that this clinically accepted combination therapy for IPAH influences the intracellular mechanical components. Conclusions: Pulmonary vasodilator drugs affect the mechanical properties of PAH-PASMCs, and there exists a mechanical effect of combination treatment on PAH-PASMCs.

Published
2021

26. Cardiac Fibroblasts Play Pathogenic Roles in Idiopathic Restrictive Cardiomyopathy

Author

Tsuru, Hirofumi, primary, Ishida, Hidekazu, additional, Narita, Jun, additional, Ishii, Ryo, additional, Suginobe, Hidehiro, additional, Ishii, Yoichiro, additional, Wang, Renjie, additional, Kogaki, Shigetoyo, additional, Taira, Masaki, additional, Ueno, Takayoshi, additional, Miyashita, Yohei, additional, Kioka, Hidetaka, additional, Asano, Yoshihiro, additional, Sawa, Yoshiki, additional, and Ozono, Keiichi, additional

Published
2021
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30. Increased Burden of Ion Channel Gene Variants Is Related to Distinct Phenotypes in Pediatric Patients With Left Ventricular Noncompaction

Author

Hirono, Keiichi, primary, Hata, Yukiko, additional, Miyao, Nariaki, additional, Okabe, Mako, additional, Takarada, Shinya, additional, Nakaoka, Hideyuki, additional, Ibuki, Keijiro, additional, Ozawa, Sayaka, additional, Origasa, Hideki, additional, Nishida, Naoki, additional, Ichida, Fukiko, additional, Takeda, Atsuhito, additional, Shimabukuro, Atsuya, additional, Akita, Chisato, additional, Fukumi, Daichi, additional, Nishihara, Eiki, additional, Tsuda, Etsuko, additional, Sakaguchi, Heima, additional, Ishida, Hidekazu, additional, Tomita, Hideshi, additional, Kise, Hiroaki, additional, Nagamine, Hiroki, additional, Uchiyama, Hiroki, additional, Katayama, Hiromi, additional, Ooki, Hiroo, additional, Nishikawa, Hiroshi, additional, Ono, Hiroshi, additional, Horigome, Hisanori Sakazaki, Hitoshi, additional, Muneuchi, Jun, additional, Yoshimoto, Jun, additional, Soumura, Junpei, additional, Kamada, Masahiro, additional, Yasuda, Kazushi, additional, Ikeda, Kazuyuki, additional, Yasuda, Keiji, additional, Kurosaki, Kenichi, additional, Mine, Kenji, additional, Ueno, Kentaro, additional, Takigiku, Kiyohiro, additional, Ogawa, Kiyoshi, additional, Inaguma, Kotaro, additional, Oyama, Kotaro, additional, Urayama, Kotaro, additional, Takahashi, Kunihiko, additional, Ohta, Kunio, additional, Nakazawa, Makoto, additional, Nakayashiro, Mami, additional, Ayusawa, Mamoro, additional, Toyono, Manatomo, additional, Nii, Masaki, additional, Miura, Masaru, additional, Fujino, Mitsuhiro, additional, Kuwabara, Naoshi, additional, Momoi, Nobuo, additional, Tsujii, Nobuyuki, additional, Motoki, Noriko, additional, Matsuo, Osamu, additional, Baba, Reizo, additional, Inuzuka, Ryo, additional, Kido, Sachiko, additional, Iwashima, Satoru, additional, Yasukochi, Satoshi, additional, Okada, Seigo, additional, Sato, Seiichi, additional, Mitsuru, Seki, additional, Kogaki, Shigetoyo, additional, Hoshino, Shinsuke, additional, Tsukano, Shinya, additional, Fujita, Shuhei, additional, Kimura, Sumito, additional, Urata, Susumu, additional, Kato, Taichi, additional, Toda, Takako, additional, Uchiyama, Takamichi, additional, Shindo, Takahiro, additional, Higaki, Takashi, additional, Kobayashi, Tomio, additional, Ozaki, Tomoyasu, additional, Tanaka, Yasuhiko, additional, Katsube, Yasuhiro, additional, Hamabuchi, Yasunobu, additional, Kajiyama, Yo, additional, Yoshida, Yoko, additional, Murakami, Yosuke, additional, Abe, Yuriko, additional, Hiraumi, Yoshimi, additional, Fukuda, Yutaka, additional, and Odanaka, Yutaka, additional

Published
2020
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33. Use of drug-coated balloon instead of drug-eluting stent for pediatric cardiac allograft vasculopathy.

Author

Hirose, Masaki, Narita, Jun, Hashimoto, Kazuhisa, Ishii, Ryo, Ishida, Hidekazu, and Ozono, Keiichi

Subjects
CARDIOVASCULAR surgery, DRUG delivery systems, PATIENT aftercare, HOMOGRAFTS, TRANSLUMINAL angioplasty, DRUG-eluting stents, CARDIOMYOPATHIES, SURGICAL stents, CORONARY restenosis, PEDIATRIC cardiology, TREATMENT effectiveness, EVEROLIMUS, CORONARY artery disease, IMMUNOSUPPRESSIVE agents, VASCULAR diseases, HEART diseases, TACROLIMUS, EQUIPMENT & supplies
Abstract

Cardiac allograft vasculopathy (CAV) sometimes leads to restenosis, even after percutaneous transcatheter intervention. Recently, drug-coated balloons (DCBs) have been successfully used to treat coronary artery disease, especially CAVs, in adults. However, no studies have used DCBs in pediatric CAVs. We encountered a patient with CAV who underwent cardiac transplantation for restrictive cardiomyopathy at the age of 2 years. Nine years after the transplantation, severe stenosis of the proximal left anterior descending branch was observed. Considering the patient's young age and the possibility of restenosis, we performed an intervention with DCB. Follow-up conducted 7 months after the intervention showed no restenosis. Cardiac coronary artery lesions following transplantation are more likely to result in restenosis earlier than arteriosclerotic lesions. In pediatric patients, restenosis might require multiple stents and prolonged antiplatelet therapy. Our findings provide evidence supporting the possibility of an effective treatment of CAV in children. [ABSTRACT FROM AUTHOR]

Published
2023
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35. GFRA2 Identifies Cardiac Progenitors and Mediates Cardiomyocyte Differentiation in a RET-Independent Signaling Pathway

Author

Ishida, Hidekazu, Saba, Rie, Kokkinopoulos, Ioannis, Hashimoto, Masakazu, Yamaguchi, Osamu, Nowotschin, Sonja, Shiraishi, Manabu, Ruchaya, Prashant, Miller, Duncan, Harmer, Stephen, Poliandri, Ariel, Kogaki, Shigetoyo, Sakata, Yasushi, Dunkel, Leo, Tinker, Andrew, Hadjantonakis, Anna-Katerina, Sawa, Yoshiki, Sasaki, Hiroshi, Ozono, Keiichi, Suzuki, Ken, and Yashiro, Kenta

Subjects
Pluripotent Stem Cells, Glial Cell Line-Derived Neurotrophic Factor Receptors, Glycosylphosphatidylinositols, Organogenesis, Receptor Protein-Tyrosine Kinases/metabolism, Ligands, Article, Mice, Cell Differentiation/physiology, Animals, Humans, Myocytes, Cardiac, lcsh:QH301-705.5, Cells, Cultured, Signal Transduction/physiology, Proto-Oncogene Proteins c-ret, Receptor Protein-Tyrosine Kinases, Cell Differentiation, Myocytes, Cardiac/metabolism, Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism, Glycosylphosphatidylinositols/metabolism, lcsh:Biology (General), Pluripotent Stem Cells/metabolism, Proto-Oncogene Proteins c-ret/metabolism, Organogenesis/physiology, Signal Transduction
Abstract

Summary A surface marker that distinctly identifies cardiac progenitors (CPs) is essential for the robust isolation of these cells, circumventing the necessity of genetic modification. Here, we demonstrate that a Glycosylphosphatidylinositol-anchor containing neurotrophic factor receptor, Glial cell line-derived neurotrophic factor receptor alpha 2 (Gfra2), specifically marks CPs. GFRA2 expression facilitates the isolation of CPs by fluorescence activated cell sorting from differentiating mouse and human pluripotent stem cells. Gfra2 mutants reveal an important role for GFRA2 in cardiomyocyte differentiation and development both in vitro and in vivo. Mechanistically, the cardiac GFRA2 signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase and its established ligands. Collectively, our findings establish a platform for investigating the biology of CPs as a foundation for future development of CP transplantation for treating heart failure., Graphical Abstract, Highlights • Gfra2 is specific for cardiac progenitors (CPs) among mesodermal cells • GFRA2 enables isolation of multipotent or unipotent CPs in mouse and human • Gfra2 and the related molecule Gfra1 play a vital role in heart development • The GFRA1/2 signal in heart development is independent of established ligands, Ishida et al. show that GPI-anchored neurotrophic factor receptor Gfra2 specifically marks cardiac progenitor cells (CPs) in mouse and human, providing a method for isolating CPs. Unexpectedly, Gfra2 plays a significant role in heart development via a non-canonical signaling pathway that is independent of known ligands and the co-receptor RET tyrosine kinase.

Published
2016

36. Fluctuations of Spleen Cytokine and Blood Lactate, Importance of Cellular Immunity in Host Defense Against Blood Stage Malaria Plasmodium yoelii

Author

Imai, Takashi, primary, Suzue, Kazutomo, additional, Ngo-Thanh, Ha, additional, Ono, Suguri, additional, Orita, Wakako, additional, Suzuki, Haruka, additional, Shimokawa, Chikako, additional, Olia, Alex, additional, Obi, Seiji, additional, Taniguchi, Tomoyo, additional, Ishida, Hidekazu, additional, Van Kaer, Luc, additional, Murata, Shigeo, additional, Tanaka, Keiji, additional, and Hisaeda, Hajime, additional

Published
2019
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39. Constitutively active form of natriuretic peptide receptor 2 ameliorates experimental pulmonary arterial hypertension

Author

Nawa, Nobutoshi, primary, Ishida, Hidekazu, additional, Katsuragi, Shinichi, additional, Baden, Hiroki, additional, Takahashi, Kunihiko, additional, Higeno, Ryota, additional, Torigoe, Fumiko, additional, Mihara, Seiko, additional, Narita, Jun, additional, Miura, Kohji, additional, Nakamura, Kazufumi, additional, Kogaki, Shigetoyo, additional, and Ozono, Keiichi, additional

Published
2016
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40. Abstract 16716: Intravascular Injection of Sendai Virus Vector Carrying Continuously cGMP Producing Mutant of Type B Natriuretic Peptide Receptor Can Ameliorate Pulmonary Arterial Hypertension

Author

Nawa, Nobutoshi, primary, Ishida, hidekazu, additional, Katuragi, Shinichi, additional, Baden, Hiroki, additional, Takahashi, Kunihiko, additional, Kogaki, Sigetoyo, additional, Higeno, Ryota, additional, Torigoe, Fumiko, additional, Mihara, Seiko, additional, Narita, Jun, additional, Miura, Koji, additional, and Ozono, Keiichi, additional

Published
2015
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41. Single-Cell Expression Profiling Reveals a Dynamic State of Cardiac Precursor Cells in the Early Mouse Embryo

Author

Kokkinopoulos, Ioannis, primary, Ishida, Hidekazu, additional, Saba, Rie, additional, Ruchaya, Prashant, additional, Cabrera, Claudia, additional, Struebig, Monika, additional, Barnes, Michael, additional, Terry, Anna, additional, Kaneko, Masahiro, additional, Shintani, Yasunori, additional, Coppen, Steven, additional, Shiratori, Hidetaka, additional, Ameen, Torath, additional, Mein, Charles, additional, Hamada, Hiroshi, additional, Suzuki, Ken, additional, and Yashiro, Kenta, additional

Published
2015
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44. An Overgrowth Disorder Associated with Excessive Production of cGMP Due to a Gain-of-Function Mutation of the Natriuretic Peptide Receptor 2 Gene

Author

Miura, Kohji, primary, Namba, Noriyuki, additional, Fujiwara, Makoto, additional, Ohata, Yasuhisa, additional, Ishida, Hidekazu, additional, Kitaoka, Taichi, additional, Kubota, Takuo, additional, Hirai, Haruhiko, additional, Higuchi, Chikahisa, additional, Tsumaki, Noriyuki, additional, Yoshikawa, Hideki, additional, Sakai, Norio, additional, Michigami, Toshimi, additional, and Ozono, Keiichi, additional

Published
2012
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50. Isogenic pairs of induced-pluripotent stem-derived endothelial cells identify DYRK1A/PPARG/EGR1 pathway is responsible for Down syndrome-associated pulmonary hypertension

Author

Suginobe, Hidehiro, Ishida, Hidekazu, Ishii, Yoichiro, Ueda, Kazutoshi, Yoshihara, Chika, Ueyama, Atsuko, Wang, Renjie, Tsuru, Hirofumi, Hashimoto, Kazuhisa, Hirose, Masaki, Ishii, Ryo, Narita, Jun, Kitabatake, Yasuji, Ozono, Keiichi, Suginobe, Hidehiro, Ishida, Hidekazu, Ishii, Yoichiro, Ueda, Kazutoshi, Yoshihara, Chika, Ueyama, Atsuko, Wang, Renjie, Tsuru, Hirofumi, Hashimoto, Kazuhisa, Hirose, Masaki, Ishii, Ryo, Narita, Jun, Kitabatake, Yasuji, and Ozono, Keiichi

Abstract

Down syndrome (DS) is the most prevalent chromosomal disorder associated with a higher incidence of pulmonary arterial hypertension (PAH). The dysfunction of vascular endothelial cells (ECs) is known to cause pulmonary arterial remodeling in PAH, although the physiological characteristics of ECs harboring trisomy 21 (T21) are still unknown. In this study, we analyzed the human vascular ECs by utilizing the isogenic pairs of T21-induced pluripotent stem cells (iPSCs) and corrected disomy 21 (cDi21)-iPSCs. In T21-iPSC-derived ECs, apoptosis and mitochondrial reactive oxygen species (mROS) were significantly increased, and angiogenesis and oxygen consumption rate (OCR) were significantly impaired as compared with cDi21-iPSC-derived ECs. The RNA-sequencing identified that EGR1 on chromosome 5 was significantly upregulated in T21-ECs. Both EGR1 suppression by siRNA and pharmacological inhibitor could recover the apoptosis, mROS, angiogenesis, and OCR in T21-ECs. Alternately, the study also revealed that DYRK1A was responsible to increase EGR1 expression via PPARG suppression, and that chemical inhibition of DYRK1A could restore the apoptosis, mROS, angiogenesis, and OCR in T21-ECs. Finally, we demonstrated that EGR1 was significantly upregulated in the pulmonary arterial ECs from lung specimens of a patient with DS and PAH. In conclusion, DYRK1A/PPARG/EGR1 pathway could play a central role for the pulmonary EC functions and thus be associated with the pathogenesis of PAH in DS., Suginobe Hidehiro, Ishida Hidekazu, Ishii Yoichiro, et al. Isogenic pairs of induced-pluripotent stem-derived endothelial cells identify DYRK1A/PPARG/EGR1 pathway is responsible for Down syndrome-associated pulmonary hypertension. Human Molecular Genetics 163, 1163 (2023); https://doi.org/10.1093/hmg/ddad162.

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