Name

AKIMOTO, Takayuki

Official Title

Professor

Affiliation

(School of Sport and Sciences)

Contact Information

URL

Web Page URL

http://www.waseda.jp/sem-muscle/index.html(Laboratory of Muscle Biology)

Grant-in-aids for Scientific Researcher Number
00323460

Sub-affiliation

Sub-affiliation

Faculty of Sport Sciences(Graduate School of Sport Sciences)

Research Council (Research Organization)/Affiliated organization(Global Education Center)

Affiliated Institutes

ヒューマンパフォーマンス研究所

研究所員 2017-2017

Paper

Detection of titin fragments in urine in response to exercise-induced muscle damage

Kanda, Kazue; Sakuma, Jun; Akimoto, Takayuki; Akimoto, Takayuki; Kawakami, Yasuo; Suzuki, Katsuhiko; Suzuki, Katsuhiko

PLoS ONE 12(7) 2017/07-2017/07

DOIScopus

Detail

Outline:© 2017 Kanda et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Many studies have attempted to determine the associations between blood biomarkers and exercise-induced muscle damage. However, poor correlations between the changes in biomarker levels and the magnitude of muscle symptoms have been reported. Recent advances in proteomic tools offer a strategy for the comprehensive analysis of protein expression, which can be used to identify biomarkers. Here, we used a proteomic analysis to identify urinary proteins that appear in response to a calf-raise exercise, including repetitive eccentric muscle contractions, and found that a titin (also known as connectin) N-terminal fragment molecule appears in the urine after eccentric exercise. We measured the titin fragment in urine samples from nine individuals before and after eccentric exercise using a newly-established enzyme-linked immunosorbent assay and found that the titin fragment excretion rate increased 96 h after the exercise (5.1 to 77.6 pg/min, p < 0.01). The changes in the titin fragment excretion rate were correlated strongly with blood markers of muscle damage and with muscle symptoms. These findings suggest that the urinary titin fragment is potentially a noninvasive biomarker of muscle damage.

Heat Stress Modulates Both Anabolic and Catabolic Signaling Pathways Preventing Dexamethasone-Induced Muscle Atrophy In Vitro

Tsuchida, Wakako;Iwata, Masahiro;Akimoto, Takayuki;Matsuo, Shingo;Asai, Yuji;Suzuki, Shigeyuki

JOURNAL OF CELLULAR PHYSIOLOGY 232(3) p.650 - 6642017-2017

PubMedDOIScopusWoS

Detail

ISSN:0021-9541

Outline:© 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc. It is generally recognized that synthetic glucocorticoids induce skeletal muscle weakness, and endogenous glucocorticoid levels increase in patients with muscle atrophy. It is reported that heat stress attenuates glucocorticoid-induced muscle atrophy; however, the mechanisms involved are unknown. Therefore, we examined the mechanisms underlying the effects of heat stress against glucocorticoid-induced muscle atrophy using C2C12 myotubes in vitro, focusing on expression of key molecules and signaling pathways involved in regulating protein synthesis and degradation. The synthetic glucocorticoid dexamethasone decreased myotube diameter and protein content, and heat stress prevented the morphological and biochemical glucocorticoid effects. Heat stress also attenuated increases in mRNAs of regulated in development and DNA damage responses 1 (REDD1) and Kruppel-like factor 15 (KLF15). Heat stress recovered the dexamethasone-induced inhibition of PI3K/Akt signaling. These data suggest that changes in anabolic and catabolic signals are involved in heat stress-induced protection against glucocorticoid-induced muscle atrophy. These results have a potentially broad clinical impact because elevated glucocorticoid levels are implicated in a wide range of diseases associated with muscle wasting. J. Cell. Physiol. 232: 650–664, 2017. © 2016 The Authors. Journal of Cellular Physiology published by Wiley Periodicals, Inc.

New mouse model of skeletal muscle atrophy using spiral wire immobilization

Onda, Akiko; Kono, Hajime; Jiao, Qibin; Akimoto, Takayuki; Miyamoto, Toshikazu; Sawada, Yasuhiro; Suzuki, Katsuhiko; Kusakari, Yoichiro; Minamisawa, Susumu; Fukubayashi, Toru

Muscle and Nerve 54(4) p.788 - 7912016/10-2016/10

PubMedDOIScopus

Detail

ISSN:0148639X

Outline:© 2016 Wiley Periodicals, Inc.Introduction: Disuse-induced skeletal muscle atrophy is a serious concern; however, there is not an effective mouse model to elucidate the molecular mechanisms. We developed a noninvasive atrophy model in mice. Methods: After the ankle joints of mice were bandaged into a bilateral plantar flexed position, either bilateral or unilateral hindlimbs were immobilized by wrapping in bonsai steel wire. Results: After 3, 5, or 10 days of immobilization of the hip, knee, and ankle, the weight of the soleus and plantaris muscles decreased significantly in both bilateral and unilateral immobilization. MAFbx/atrogin-1 and MuRF1 mRNA was found to have significantly increased in both muscles, consistent with disuse-induced atrophy. Notably, the procedure did not result in either edema or necrosis in the fixed hindlimbs. Conclusions: This method allows repeated, direct access to the immobilized muscle, making it a useful procedure for concurrent application and assessment of various therapeutic interventions. Muscle Nerve 54: 788–791, 2016.

MRF4 negatively regulates adult skeletal muscle growth by repressing MEF2 activity

Moretti, Irene; Ciciliot, Stefano; Dyar, Kenneth A.; Abraham, Reimar; Murgia, Marta; Murgia, Marta; Agatea, Lisa; Akimoto, Takayuki; Akimoto, Takayuki; Bicciato, Silvio; Forcato, Mattia; Pierre, Philippe; Pierre, Philippe; Uhlenhaut, N. Henriette; Rigby, Peter W J; Carvajal, Jaime J.; Blaauw, Bert; Blaauw, Bert; Calabria, Elisa; Calabria, Elisa; Schiaffino, Stefano

Nature Communications 72016/08-2016/08

DOIScopus

Detail

Outline:© The Author(s) 2016.The myogenic regulatory factor MRF4 is highly expressed in adult skeletal muscle but its function is unknown. Here we show that Mrf4 knockdown in adult muscle induces hypertrophy and prevents denervation-induced atrophy. This effect is accompanied by increased protein synthesis and widespread activation of muscle-specific genes, many of which are targets of MEF2 transcription factors. MEF2-dependent genes represent the top-ranking gene set enriched after Mrf4 RNAi and a MEF2 reporter is inhibited by co-transfected MRF4 and activated by Mrf4 RNAi. The Mrf4 RNAi-dependent increase in fibre size is prevented by dominant negative MEF2, while constitutively active MEF2 is able to induce myofibre hypertrophy. The nuclear localization of the MEF2 corepressor HDAC4 is impaired by Mrf4 knockdown, suggesting that MRF4 acts by stabilizing a repressor complex that controls MEF2 activity. These findings open new perspectives in the search for therapeutic targets to prevent muscle wasting, in particular sarcopenia and cachexia.

Patent

Reference Number:907

抗筋委縮剤(日本)

秋本 崇之

2009- 28836、2010-184879

Research Grants & Projects

Grant-in-aids for Scientific Research Adoption Situation

Research Classification:

Development of fluorescent probe for glucose uptake into skeletal muscle

2017/-0-2019/-0

Allocation Class:¥6500000

Research Classification:

Role of microRNAs in exercise-induced angiogenesis

2016/-0-2019/-0

Allocation Class:¥17550000

Research Classification:

development of in vivo imaging system for skeletal muscle biology

2014/-0-2016/-0

Allocation Class:¥3640000

Research Classification:

The mechanism underlying sleep disorder-induced decrease in athletic performance and its improvement

2014/-0-2017/-0

Allocation Class:¥15990000

Research Classification:

The role of microRNAs in mechanical stress-induced muscle adaptation

2013/-0-2016/-0

Allocation Class:¥18850000

Research Classification:

Effect of mechanical stress on stemness of embryonic stem cells

2011/-0-2014/-0

Allocation Class:¥3640000

Research Classification:

Development of novel biomarkers on exercise, stress and aging

2011/-0-2015/-0

Allocation Class:¥49010000

Research Classification:

Monitoring stress protein in saliva to prevent impairment of physical condition in athletes and elderly individuals

2010/-0-2014/-0

Allocation Class:¥18200000

Research Classification:

Functional analysis of mechanical stress-induced microRNAs

Allocation Class:¥27950000

Research Classification:

Local muscular steroidogenesis and exercise for anti-aging

Allocation Class:¥17810000

Research Classification:

The effects of exercise on immune senescence in elderly

Allocation Class:¥18590000

Research Classification:

Regulation of mesenchymal cell differentiation by mechanical stress via PGC-1a

Allocation Class:¥28600000

Research Classification:

Development of the personalized health promotion program for the prevention of life-style related disease : Contribution of Cardiorespiratory Fitness and Obesity Genes to the Risk Factors of Metabolic Syndrome

Allocation Class:¥4140000

Research Classification:

An analysis of the non-contact anterior cruciate ligament injury

Allocation Class:¥3600000

Research Classification:

Development of a SIgA measurement kit for monitoring of risk of URTI

Allocation Class:¥5700000

On-campus Research System

Special Research Project

組織への糖取り込みをリアルタイム観察可能な蛍光プローブの開発

2016

Research Results Outline:最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリック最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリックシンドローム等の代謝性疾患を防ぐ手段となり得る事が明らかになってきた.特に,骨格筋は最大の血糖処理...最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリックシンドローム等の代謝性疾患を防ぐ手段となり得る事が明らかになってきた.特に,骨格筋は最大の血糖処理器官であり,糖のみならず脂質代謝にも重要な働きをしていることから,骨格筋におけるインスリン作用の不全,すなわちインスリン抵抗性は糖尿病をはじめとする多くの生活習慣病の発症基盤となっていると考えられる.本研究では,骨格筋組織の糖取り込み機構について解析するために,まず組織工学技術を応用した筋組織の三次元培養法を確立を試みた.その結果,脱細胞化ブダ大動脈を人工腱として利用し,コラーゲンゲルを基質とした筋芽細胞の三次元培養によって,in vitroで人工筋組織を作製する事に成功した.今後は,作製中の蛍光プローブを用いて,人工筋組織での糖取り込みを観察する.

三次元培養人工骨格筋組織を用いた糖取り込み機構の解析

2016

Research Results Outline:最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリック最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリックシンドローム等の代謝性疾患を防ぐ手段となり得る事が明らかになってきた.特に,骨格筋は最大の血糖処理...最近,骨格筋におけるイベントが筋局所だけでなく全身の代謝調節に係っている事が明らかになるとともに,筋機能の維持が近年大きな問題になっているメタボリックシンドローム等の代謝性疾患を防ぐ手段となり得る事が明らかになってきた.特に,骨格筋は最大の血糖処理器官であり,糖のみならず脂質代謝にも重要な働きをしていることから,骨格筋におけるインスリン作用の不全,すなわちインスリン抵抗性は糖尿病をはじめとする多くの生活習慣病の発症基盤となっていると考えられる.本研究では,骨格筋組織の糖取り込み機構について解析するために,まず組織工学技術を応用した筋組織の三次元培養法を確立を試みた.その結果,脱細胞化ブダ大動脈を人工腱として利用し,コラーゲンゲルを基質とした筋芽細胞の三次元培養によって,in vitroで人工筋組織を作製する事に成功した.今後は,作製中の蛍光プローブを用いて,人工筋組織での糖取り込みを観察する.

老化の制御におけるマイクロRNAの役割

2019

Research Results Outline: すでに超高齢社会を迎えた我が国を含め,先進諸国において人口の高齢化が進んでおり,高齢者の健康問題のみならず介護・医療費の増加による経済的負担の増加, すでに超高齢社会を迎えた我が国を含め,先進諸国において人口の高齢化が進んでおり,高齢者の健康問題のみならず介護・医療費の増加による経済的負担の増加,生産年齢人口の低下等が大きな社会課題となっており,これらに対応することが世界的にも喫緊の課題となっ... すでに超高齢社会を迎えた我が国を含め,先進諸国において人口の高齢化が進んでおり,高齢者の健康問題のみならず介護・医療費の増加による経済的負担の増加,生産年齢人口の低下等が大きな社会課題となっており,これらに対応することが世界的にも喫緊の課題となっている.このような超高齢社会の到来の中で,「老化」の生物学的本質やそのプロセスに関する科学的なエビデンスがこれまで以上に注目されている.老化の原因を解明することで,老化関連疾病の対策発見が期待でき,介護や医療に費やされる社会保障費の削減のためにも必要であると考えられる.老化の原因に関する仮説(老化仮説)として,プログラム説,活性酸素説,テロメア説,遺伝子修復エラー説など様々な仮説が提案されているものの,高等生物の動物個体における老化を説明できる仮説は存在せず,老化の原因はいまだ解明されていない.本研究では,我々の研究室で作製したあるマイクロRNAの遺伝子改変マウスにおいて偶然見出された「老化加速」表現型を解析するための予備的な検討を行った.

Lecture Course

Course TitleSchoolYearTerm
Seminar I (Muscle Biology)School of Sport Sciences2020fall semester
Seminar II (Muscle Biology)School of Sport Sciences2020spring semester
Seminar III (Muscle Biology)School of Sport Sciences2020fall semester
Seminar IV (Muscle Biology)School of Sport Sciences2020spring semester
Basic ScienceSchool of Sport Sciences2020spring semester
Basic Seminar of Sport Medicine and ScienceSchool of Sport Sciences2020spring semester
PhysiologySchool of Sport Sciences2020spring semester
BiochemistrySchool of Sport Sciences2020spring semester
Molecular BiologySchool of Sport Sciences2020fall semester
Muscle Biology (Directed Research M) AGraduate School of Sport Sciences2020spring semester
Muscle Biology (Directed Research M) BGraduate School of Sport Sciences2020fall semester
Health and Exercise Science 1 (Directed Research M) (Akimoto) AGraduate School of Sport Sciences2020fall semester
Health and Exercise Science 1 (Directed Research M) (Akimoto) BGraduate School of Sport Sciences2020spring semester
Muscle Biology (Seminar 1) AGraduate School of Sport Sciences2020spring semester
Muscle Biology (Seminar 1) BGraduate School of Sport Sciences2020fall semester
Health and exercise science 1 (Seminar 1) AGraduate School of Sport Sciences2020spring quarter
Health and exercise science 1 (Seminar 1) BGraduate School of Sport Sciences2020summer quarter
Health and exercise science 1 (Seminar 2) AGraduate School of Sport Sciences2020fall quarter
Health and exercise science 1 (Seminar 2) BGraduate School of Sport Sciences2020winter quarter
Muscle Biology (Seminar 2) AGraduate School of Sport Sciences2020spring semester
Muscle Biology (Seminar 2) BGraduate School of Sport Sciences2020fall semester
Fundamentals of Life ScienceGraduate School of Sport Sciences2020fall quarter
Muscle Biology (Directed Research D) AGraduate School of Sport Sciences2020spring semester
Muscle Biology (Directed Research D) BGraduate School of Sport Sciences2020fall semester
Sport Sciences 1 01Global Education Center2020spring quarter
Sport Sciences 2 01Global Education Center2020summer quarter