PMID- 30209036
OWN - NLM
STAT- MEDLINE
DCOM- 20190826
LR  - 20190826
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 132
IP  - 19
DP  - 2018 Oct 15
TI  - Local cyclical compression modulates macrophage function in situ and alleviates 
      immobilization-induced muscle atrophy.
PG  - 2147-2161
LID - 10.1042/CS20180432 [doi]
AB  - Physical inactivity gives rise to numerous diseases and organismal dysfunctions, 
      particularly those related to aging. Musculoskeletal disorders including muscle 
      atrophy, which can result from a sedentary lifestyle, aggravate locomotive 
      malfunction and evoke a vicious circle leading to severe functional disruptions 
      of vital organs such as the brain and cardiovascular system. Although the 
      significance of physical activity is evident, molecular mechanisms behind its 
      beneficial effects are poorly understood. Here, we show that massage-like 
      mechanical interventions modulate immobilization-induced pro-inflammatory 
      responses of macrophages in situ and alleviate muscle atrophy. Local cyclical 
      compression (LCC) on mouse calves, which generates intramuscular pressure waves 
      with amplitude of 50 mmHg, partially restores the myofiber thickness and 
      contracting forces of calf muscles that are decreased by hindlimb immobilization. 
      LCC tempers the increase in the number of cells expressing pro-inflammatory 
      proteins, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 (MCP-1), 
      including macrophages in situ The reversing effect of LCC on 
      immobilization-induced thinning of myofibers is almost completely nullified when 
      macrophages recruited from circulating blood are depleted by administration of 
      clodronate liposomes. Furthermore, application of pulsatile fluid shear stress, 
      but not hydrostatic pressure, reduces the expression of MCP-1 in macrophages in 
      vitro Together with the LCC-induced movement of intramuscular interstitial fluid 
      detected by microCT analysis, these results suggest that mechanical modulation of 
      macrophage function is involved in physical inactivity-induced muscle atrophy and 
      inflammation. Our findings uncover the implication of mechanosensory function of 
      macrophages in disuse muscle atrophy, thereby opening a new path to develop a 
      novel therapeutic strategy utilizing mechanical interventions.
CI  - (c) 2018 The Author(s).
FAU - Saitou, Kumiko
AU  - Saitou K
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
AD  - Graduate School of Sport Sciences, Waseda University, 2-579-15 Mikajima, 
      Tokorozawa, Saitama 359-1192, Japan.
FAU - Tokunaga, Masakuni
AU  - Tokunaga M
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Yoshino, Daisuke
AU  - Yoshino D
AD  - Frontier Research Institute for Interdisciplinary Sciences, Tohoku University, 
      6-3 Aramaki-aza-Aoba, Aoba, Sendai, Miyagi 980-8578, Japan.
FAU - Sakitani, Naoyoshi
AU  - Sakitani N
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Maekawa, Takahiro
AU  - Maekawa T
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Ryu, Youngjae
AU  - Ryu Y
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Nagao, Motoshi
AU  - Nagao M
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Nakamoto, Hideki
AU  - Nakamoto H
AD  - Department of Orthopaedic Surgery, Graduate School of Medicine, The University of 
      Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan.
FAU - Saito, Taku
AU  - Saito T
AD  - Department of Orthopaedic Surgery, Graduate School of Medicine, The University of 
      Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan.
FAU - Kawanishi, Noriaki
AU  - Kawanishi N
AD  - Faculty of Advanced Engineering, Chiba Institute of Technology, 2-1-1 Shibazono, 
      Narashino, Chiba 275-0023, Japan.
FAU - Suzuki, Katsuhiko
AU  - Suzuki K
AD  - Faculty of Sport Sciences, Waseda University, 2-579-15 Mikajima, Tokorozawa, 
      Saitama 359-1192, Japan.
FAU - Ogata, Toru
AU  - Ogata T
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Makuuchi, Michiru
AU  - Makuuchi M
AD  - Section of Neuropsychology, National Rehabilitation Center for Persons with 
      Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Takashima, Atsushi
AU  - Takashima A
AD  - Department of Assistive Technology, National Rehabilitation Center for Persons 
      with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
FAU - Sawada, Keisuke
AU  - Sawada K
AD  - Department of Pathology, Cell Pathology Division, The Children's Hospital of 
      Philadelphia, Philaldelphia, PA 19104, U.S.A.
FAU - Kawamura, Shunsuke
AU  - Kawamura S
AD  - Department of Biosystems Science and Engineering, ETH Zurich, Mattenstrasse 26, 
      Basel 4058, Switzerland.
FAU - Nakazato, Koichi
AU  - Nakazato K
AD  - Graduate School of Health and Sport Sciences, Nippon Sport Science University, 
      7-1-1 Fukasawa, Setagaya, Tokyo 158-8508, Japan.
FAU - Kouzaki, Karina
AU  - Kouzaki K
AD  - Graduate School of Health and Sport Sciences, Nippon Sport Science University, 
      7-1-1 Fukasawa, Setagaya, Tokyo 158-8508, Japan.
FAU - Harada, Ichiro
AU  - Harada I
AD  - Nadogaya Institute, Nadogaya Hospital, 687-4 Nadogaya, Kashiwa, Chiba 277-0032, 
      Japan.
FAU - Ichihara, Yoshinori
AU  - Ichihara Y
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
AD  - Division of Pharmacology, Faculty of Medicine, Tottori University, 86 Nishi-cho, 
      Yonago, Tottori 683-8503, Japan.
FAU - Sawada, Yasuhiro
AU  - Sawada Y
AD  - Department of Rehabilitation for Motor Functions, National Rehabilitation Center 
      for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan 
      ys454-ind@umin.ac.jp.
AD  - Department of Clinical Research, National Rehabilitation Center for Persons with 
      Disabilities, 4-1 Namiki, Tokorozawa, Saitama 359-8555, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181012
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (Chemokine CCL2)
RN  - 0 (Tumor Necrosis Factor-alpha)
EIN - Clin Sci (Lond). 2019 Feb 5;133(3):407. PMID: 30723116
MH  - Animals
MH  - Chemokine CCL2/metabolism
MH  - Female
MH  - Hindlimb Suspension/physiology
MH  - Macrophages/metabolism/*physiology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Muscle Fibers, Skeletal/metabolism/*physiology
MH  - Muscle, Skeletal/metabolism/*physiopathology
MH  - Muscular Atrophy/metabolism/*physiopathology
MH  - *Stress, Mechanical
MH  - Tumor Necrosis Factor-alpha/metabolism
OTO - NOTNLM
OT  - disuse muscle atrophy
OT  - fluid shear stress
OT  - interstitial fluid
OT  - macrophage
OT  - massage
OT  - physical inactivity
EDAT- 2018/09/14 06:00
MHDA- 2019/08/27 06:00
CRDT- 2018/09/14 06:00
PHST- 2018/07/14 00:00 [received]
PHST- 2018/09/10 00:00 [revised]
PHST- 2018/09/11 00:00 [accepted]
PHST- 2018/09/14 06:00 [pubmed]
PHST- 2019/08/27 06:00 [medline]
PHST- 2018/09/14 06:00 [entrez]
AID - CS20180432 [pii]
AID - 10.1042/CS20180432 [doi]
PST - epublish
SO  - Clin Sci (Lond). 2018 Oct 12;132(19):2147-2161. doi: 10.1042/CS20180432. Print 
      2018 Oct 15.