Updated on 2024/03/07

写真a

 
Matusmoto Tae
 
Affiliation
Tamanagayama Hospital, Department of Pediatrics, Professor
Title
Professor
External link

Degree

  • 医学博士 ( 日本医科大学大学院 )

Research Interests

  • 小児医療

  • 包括的性教育

  • hypophosphatasia

  • gene therapy

Research Areas

  • Life Science / Embryonic medicine and pediatrics  / pediatrics

Education

  • Nippon Medical School   Medical School

    1993.4 - 1999.3

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Research History

  • Nippon Medical School   pediatrics department   Associate Professor

    2023.10

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Professional Memberships

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Papers

  • Treatment with bone maturation and average lifespan of HPP model mice by AAV8-mediated neonatal gene therapy via single muscle injection Reviewed

    Tae Matsumoto, Koichi Miyake, Noriko Miyake, Osamu Iijima, Kumi Adachi, Sonoko Narisawa, José Luis Millán, Hideo Orimo, Takashi Shimada

    Molecular Therapy Methods and Clinical Development   12 ( 22 )   330 - 337   2021.6

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

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  • Successful Gene Therapy in Utero for Lethal Murine Hypophosphatasia Reviewed

    Hanako Sugano, Tae Matsumoto, Koichi Miyake, Atsushi Watanabe, Osamu Iijima, Makoto Migita, Sonoko Narisawa, Jose Luis Millan, Yoshitaka Fukunaga, Takashi Shimada

    HUMAN GENE THERAPY   23 ( 4 )   399 - 406   2012.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：MARY ANN LIEBERT INC  

    Hypophosphatasia (HPP), caused by mutations in the gene ALPL encoding tissue-nonspecific alkaline phosphatase (TNALP), is an inherited systemic skeletal disease characterized by mineralization defects of bones and teeth. The clinical severity of HPP varies widely, from a lethal perinatal form to mild odontohypophosphatasia showing only dental manifestations. HPP model mice (Akp2(-/-)) phenotypically mimic the severe infantile form of human HPP; they appear normal at birth but die by 2 weeks of age because of growth failure, hypomineralization, and epileptic seizures. In the present study, we investigated the feasibility of fetal gene therapy using the lethal HPP model mice. On day 15 of gestation, the fetuses of HPP model mice underwent transuterine intraperitoneal injection of adeno-associated virus serotype 9 (AAV9) expressing bone-targeted TNALP. Treated and delivered mice showed normal weight gain and seizure-free survival for at least 8 weeks. Vector sequence was detected in systemic organs including bone at 14 days of age. ALP activities in plasma and bone were consistently high. Enhanced mineralization was demonstrated on X-ray images of the chest and forepaw. Our data clearly demonstrate that systemic injection of AAV9 in utero is an effective strategy for the treatment of lethal HPP mice. Fetal gene therapy may be an important choice after prenatal diagnosis of life-threatening HPP.

    DOI： 10.1089/hum.2011.148

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  • Rescue of Severe Infantile Hypophosphatasia Mice by AAV-Mediated Sustained Expression of Soluble Alkaline Phosphatase Reviewed

    Tae Matsumoto, Koichi Miyake, Seiko Yamamoto, Hideo Orimo, Noriko Miyake, Yuko Odagaki, Kumi Adachi, Osamu Iijima, Sonoko Narisawa, Jose Luis Millan, Yoshitaka Fukunaga, Takashi Shimada

    HUMAN GENE THERAPY   22 ( 11 )   1355 - 1364   2011.11

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：MARY ANN LIEBERT INC  

    Hypophosphatasia (HPP) is an inherited disease caused by a deficiency of tissue-nonspecific alkaline phosphatase (TNALP). The major symptom of human HPP is hypomineralization, rickets, or osteomalacia, although the clinical severity is highly variable. The phenotypes of TNALP knockout (Akp2(-/-)) mice mimic those of the severe infantile form of HPP. Akp2(-/-) mice appear normal at birth, but they develop growth failure, epileptic seizures, and hypomineralization and die by 20 days of age. Previously, we have shown that the phenotype of Akp2(-/-) mice can be prevented by enzyme replacement of bone-targeted TNALP in which deca-aspartates are linked to the C-terminus of soluble TNALP (TNALP-D10). In the present study, we evaluated the therapeutic effects of adeno-associated virus serotype 8 (AAV8) vectors that express various forms of TNALP, including TNALP-D10, soluble TNALP tagged with the Flag epitopes (TNALP-F), and native glycosylphosphatidylinositol-anchored TNALP (TNALP-N). A single intravenous injection of 5 x 10(10) vector genomes of AAV8-TNALP-D10 into Akp2(-/-) mice at day 1 resulted in prolonged survival and phenotypic correction. When AAV8-TNALP-F was injected into neonatal Akp2(-/-) mice, they also survived without epileptic seizures. Interestingly, survival effects were observed in some animals treated with AAV8-TNALP-N. All surviving Akp2(-/-) mice showed a healthy appearance and a normal activity with mature bone mineralization on X-rays. These results suggest that sustained alkaline phosphatase activity in plasma is essential and sufficient for the rescue of Akp2(-/-) mice. AAV8-mediated systemic gene therapy appears to be an effective treatment for the infantile form of human HPP.

    DOI： 10.1089/hum.2010.210

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  • Prolonged Survival and Phenotypic Correction of Akp2(-/-) Hypophosphatasia Mice by Lentiviral Gene Therapy Reviewed

    Seiko Yamamoto, Hideo Orimo, Tae Matsumoto, Osamu Iijima, Sonoko Narisawa, Takahide Maeda, Jose Luis Millan, Takashi Shimada

    JOURNAL OF BONE AND MINERAL RESEARCH   26 ( 1 )   135 - 142   2011.1

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

    Hypophosphatasia (HPP) is an inherited systemic skeletal disease caused by mutations in the gene encoding the tissue-nonspecific alkaline phosphatase (TNALP) isozyme. The clinical severity of HPP varies widely, with symptoms including rickets and osteomalacia. TNALP knockout (Akp2(-/-)) mice phenotypically mimic the severe infantile form of HPP; that is, TNALP-deficient mice are born with a normal appearance but die by 20 days of age owing to growth failure, hypomineralization, and epileptic seizures. In this study, a lentiviral vector expressing a bone-targeted form of TNALP was injected into the jugular vein of newborn Akp2(-/-) mice. We found that alkaline phosphatase activity in the plasma of treated Akp2(-/-) mice increased and remained at high levels throughout the life of the animals. The treated Akp2(-/-) mice survived for more than 10 months and demonstrated normal physical activity and a healthy appearance. Epileptic seizures were completely inhibited in the treated Akp2(-/-) mice, and X-ray examination of the skeleton showed that mineralization was significantly improved by the gene therapy. These results show that severe infantile HPP in TNALP knockout mice can be treated with a single injection of lentiviral vector during the neonatal period. (C) 2011 American Society for Bone and Mineral Research.

    DOI： 10.1002/jbmr.201

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  • Renal Biopsy-induced Hematoma and Infection in a Patient with Asymptomatic May-Hegglin Anomaly Reviewed

    Tae Matsumoto, Takeshi Yanagihara, Kaoru Yoshizaki, Masami Tsuchiya, Mika Terasaki, Kiyotaka Nagahama, Akira Shimizu, Shinji Kunishima, Miho Maeda

    Journal of Nippon Medical School   88 ( 6 )   579 - 584   2021.12

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

    The May-Hegglin anomaly is characterized by inherited thrombocytopenia, giant platelets, and leukocyte cytoplasmic inclusion bodies. The Fechtner, Sebastian, and Epstein syndromes are associated with mutations of the MYH9-coding nonmuscle myosin heavy chain IIA, similar to the May-Hegglin anomaly, and are together classified as MYH9 disorders. MYH9 disorders may include symptoms of Alport syndrome, including nephritis and auditory and ocular disorders. A 6-year-old boy was diagnosed with an MYH9 disorder after incidental discovery of hematuria and proteinuria. Focal segmental glomerulosclerosis was detected on renal biopsy. However, despite no prior bleeding diatheses, he developed a large post-biopsy hematoma despite a preprocedural platelet transfusion calculated to increase the platelet count from 54,000/μL to >150,000/μL. Idiopathic thrombocytopenic purpura is a major cause of pediatric thrombocytopenia following acute infection or vaccination, and patients with MYH9 disorders may be misdiagnosed with idiopathic thrombocytopenic purpura and inappropriately treated with corticosteroids. Careful differential diagnosis is important in thrombocytopenic patients with hematuria and proteinuria for the early detection of thrombocytopenia. Patients with MYH9 disorders require close follow-up and treatment with angiotensin II receptor blockers to prevent the onset of progressive nephritis, which may necessitate hemodialysis or renal transplantation. The need for renal biopsy in patients with MYH9 disorders should be carefully considered because there could be adverse outcomes even after platelet transfusion.

    DOI： 10.1272/jnms.JNMS.2021_88-609

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  • Cholelithiasis in a Patient with Type 2 Gaucher Disease Reviewed

    Makoto Migita, Sakae Kumasaka, Tae Matsumoto, Hanako Tajima, Takahiro Ueda, Atsuyuki Yamataka

    JOURNAL OF NIPPON MEDICAL SCHOOL   81 ( 1 )   40 - 42   2014.2

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：MEDICAL ASSOC NIPPON MEDICAL SCH  

    Gaucher disease is an autosomal recessively inherited lysosomal storage disease in which a deficiency of glucocerebrosidase is associated with the accumulation of glucocerebroside in reticuloendothelial cells. Clinically, 3 types of Gaucher disease have been defined on the basis of the presence or absence of neurological symptoms. The frequency of gallbladder involvement is reportedly greater in patients with type 1 Gaucher disease than in healthy persons. We report a case of recurrent cholelithiasis and liver failure in a patient with type 2 Gaucher disease who showed severe progressive neurological involvement.

    DOI： 10.1272/jnms.81.40

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  • PRSS1およびSPINK1遺伝子異常による小児期急性膵炎の臨床的特徴とその管理

    鈴木光幸, 成高中之, 箕輪圭, 木下達也, 中村蓉子, 中西直之, 宮下律子, 浜武継, 渡邉誠, 松本多絵, 横山孝二, 鍋島泰典, 蟹江健介, 藤野明浩, 清水俊明

    日本小児栄養消化器肝臓学会雑誌   26 ( 1 )   12 - 20   2012.9

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    Language：Japanese  

    J-GLOBAL

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  • A case of acute mitral regurgitation due to ruptured chordae tendineae, showed unilateral diffuse pulmonary infiltration

    HAYASHI Hatsuka, UMEHARA Minoru, MATSUMOTO Tae, NAGAFUCHI Hiroyuki, HAYASHI Kenichi, ASOU Toshihide, KAWATAKI Motoyoshi

    JJPP   18 ( 1 )   20 - 24   2007.6

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    Language：Japanese   Publisher：日本小児呼吸器疾患学会  

    We reported a case of mitral regurgitation due to ruptured chordae tendineae, showed unilateral diffuse pulmonary infiltration on chest X-ray film on admission. Five-month-old boy was transferred to our hospital because of severe respiratory distress. He had vomiting and cough before progression of respiratory distress and initial diagnosis was aspiration pneumonia. We treated him with antibiotics and respiratory support, including mechanical ventilation, but his cardiopulmonary condition became worse. Three dimensional echocardiography revealed mitral regurgitation due to ruptured chordae tendineae as the cause of heart failure. His condition finally recovered after mitral valve plasty and mitral plication. We concluded that such a cardiogenic mechanism should be reminded in cases with unilateral diffuse pulmonary infiltration.

    DOI： 10.5701/jjpp.18.20

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    Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2007&ichushi_jid=J02564&link_issn=&doc_id=20070710060004&doc_link_id=%2Fcq7pedia%2F2007%2F001801%2F004%2F0020-0024%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcq7pedia%2F2007%2F001801%2F004%2F0020-0024%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • Transient cardiomyopathy in a patient with congenital contractural arachnodactyly (Beals syndrome) Reviewed

    Tae Matsumoto, Atsushi Watanabe, Makoto Migita, Yoshihiro Gocho, Jun Hayakawa, Shun-Ichi Ogawa, Takashi Shimada, Yoshitaka Fukunaga

    Journal of Nippon Medical School   73 ( 5 )   285 - 288   2006.10

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    Language：English   Publishing type：Research paper (scientific journal)  

    We report on an infant with Beals syndrome (congenital contractural arachnodactyly [CCA], MIM 121050) with transient cardiomyopathy showing ballon-like dilatation of the left ventricle that was similar to noncompaction. The patient's father and two of his brothers were also found to have CCA without cardiovascular complications. CCA, which is caused by a mutation of the gene for fibrillin 2 protein is similar to Marfan syndrome (MIM 154700), which is caused by a mutation of fibrillin 1 but produces a life-threatening cardiovascular complications. This is the first report of CCA with transient cardiomyopathy. We discuss the mechanism of the spontaneous improvement of cardiomyopathy in this case on the basis of expression of the responsible gene.

    DOI： 10.1272/jnms.73.285

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  • Solid and cystic tumor of the pancreas in a 12-year-old boy Reviewed

    T Asano, T Matsumoto, CL Zhi, M Maeda, E Uchida, T Tajiri, Y Fukunaga

    PEDIATRICS INTERNATIONAL   45 ( 3 )   339 - 341   2003.6

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING ASIA  

    DOI： 10.1046/j.1442-200X.2003.01729.x

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  • Genetic diagnosis of Werdnig-Hoffmann disease: A problem for application to prenatal diagnosis Reviewed

    Makoto Migita, Yohko Uchikoba, Hideo Orimo, Takashi Shimada, Tae Matsumoto, Jun Hayakawa, Osamu Fujino, Makiko Saitoh, Yoshitaka Fukunaga

    Journal of Nippon Medical School   70 ( 1 )   45 - 48   2003

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Medical Association of Nippon Medical School  

    We report a floppy infant with Werdnig-Hoffmann disease (spinal muscular atrophy: SMA type 1) and Klinefelter syndrome. After genetic counseling with parents, a genetic diagnosis using DNA from the infant's peripheral blood mononuclear cells was performed. The parents' deletion of exons 7 and 8 of the survival motor neuron (smn) gene and exons 4 and 5 of the neuronal apoptosis inhibitory protein (naip) gene were noted in the infant, so he was confirmed to have SMA type 1. The parents wanted to receive a prenatal diagnosis on the next pregnancy. However this genetic test is achieved by confirming that a specific band can not be detected by PCR. Therefore, this method should be applied with great care to prenatal diagnosis using chorionic villi, which may be contaminated with maternal tissue.

    DOI： 10.1272/jnms.70.45

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  • Fetal Inflammatory Response Syndrome and Neonatal Complications

    SHIMA Yoshio, NISHIMAKI Shigeru, FUJITA Atsushi, BABA Chiaki, ORIMOTO Mizue, FUJIMURA Juri, MATSUMOTO Tae

    日本新生児学会雑誌   38 ( 4 )   743 - 747   2002.12

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    Language：Japanese  

    CiNii Books

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  • Hemolytic Anemia of Unknown Origin in Four Very Low Birth Weight Infants

    MATSUMOTO T, SHIMA Y, TAKECHI N, KAWABATA K, FUJIMURA J

    日本新生児学会雑誌   38 ( 4 )   713 - 717   2002.12

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    Language：Japanese  

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  • A case of neonatal immature retroperitoneal teratoma. Reviewed

    Tae Matusmoto

    Surgery in childhood international   9 ( 3 )   157 - 159   2001.3

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  • Two cases of influenza with impaired ocular movement Reviewed

    Makoto Migita, Tae Matsumoto, Osamu Fujino, Yasuko Takaishi, Nobuhiro Yuki, Yoshitaka Fukunaga

    European Journal of Paediatric Neurology   5 ( 2 )   83 - 85   2001

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：W.B. Saunders Ltd  

    Complications of influenza include respiratory disorders (pneumonia, bronchitis and croup) and occasionally myocarditis, myositis, encephalitis, encephalopathy and Reye's syndrome, which may be life-threatening and cause various sequelae. We report two patients who developed unusual complications of influenza infection: one had ptosis and impaired ocular movement, and the other suffered from Guillain-Barré syndrome with paralysis of the extraocular muscles.

    DOI： 10.1053/ejpn.2001.0470

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  • 診断,治療方針決定に難渋した後腹膜原発の未熟奇形腫の乳児例

    川畑 建, 右田 真, 松本 多絵, 植田 高弘, 福永 慶隆, 林 瑞成, 小林 弘幸, 山高 篤行, 宮野 武

    日本新生児学会雑誌   36 ( 2 )   135 - 135   2000.6

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    Language：Japanese   Publisher：(一社)日本周産期・新生児医学会  

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Books

  • The Art of Travel and Global Health

    （ Role： Contributorpediatric patient, allegy）

    2017.9  （ ISBN:4525233818 ）

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    Total pages：306  

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Misc.

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Presentations

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Research Projects

  • Development of a Novel Gene Therapy for Hypophosphatasia

    Grant number：1202308  2023.4 - 2026.4

    AMED 

    Miyake koichi, Matsumoto Tae, Matsuyama Kotone

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    Authorship：Coinvestigator(s) 

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  • Development of gene therapy for hypophosphatasia

    Grant number：20K08268  2020.4 - 2021.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

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    Grant amount：\4420000 （ Direct Cost: \3400000 、 Indirect Cost：\1020000 ）

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  • The gene therapy for hypophosphatasia animal model

    Grant number：15K09605  2015.4 - 2019.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Matsumoto Tae, Miyake Koichi

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    Authorship：Principal investigator  Grant type：Competitive

    Grant amount：\4810000 （ Direct Cost: \3700000 、 Indirect Cost：\1110000 ）

    Hypophosphatasia is an inherited skeletal disease characterized by defective bone and teeth mineralization due to the deficiency of tissue-nonspecific alkaline phosphatase (TNALP), which leads to abnormal mineralization of skeletal and dental tissues. TNALP knockout (Akp2-/-) mice are good models for infantile HPP.We used a single intramuscular injection of Adeno associated vector type 8 (AAV8)with a bone-targeted form of human TNALP in which a deca-aspartate sequence is linked to the C terminal end of soluble TNALP (TNALP-D10) to prolong Akp2-/- mice life with insufficient bone maturity.Treated Akp2-/- mice with AAV8-TNALP-D10 lived longer than 1 year with normal physical activity and healthy appearance, while control Akp2-/- mice died in 3 weeks. At 18 months, bone mineral density and bone volume/tissue volume values were close to those of control ones. The success of intramuscular gene therapy for Akp2-/- mice with AAV8-TNALP-D10 shows possibility to achieve human therapy.

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Teaching Experience

  • Pediatrics Department

    2023.7
    Institution：Nippon Medical School

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  • pediatrics

    2018.4
    Institution：University of Tokyo Health Sciences

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  • 小児科学

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