Implication of anti-inflammatory macrophages in regenerative moto-neuritogenesis

Promotion of myoblast migration and neural chemorepellent semaphorin 3A expression in injured muscle

Shohei Sakaguchi, Jun Ichi Shono, Takahiro Suzuki, Shoko Sawano, Judy E. Anderson, Mai Khoi Q. Do, Hideaki Ohtsubo, Wataru Mizunoya, Yusuke Sato, Mako Nakamura, Mitsuhiro Furuse, Koji Yamada, Yoshihide Ikeuchi, Ryuichi Tatsumi

研究成果: ジャーナルへの寄稿記事

24 引用 (Scopus)

抄録

Regenerative mechanisms that regulate intramuscular motor innervation are thought to reside in the spatiotemporal expression of axon-guidance molecules. Our previous studies proposed a heretofore unexplored role of resident myogenic stem cell (satellite cell)-derived myoblasts as a key presenter of a secreted neural chemorepellent semaphorin 3A (Sema3A); hepatocyte growth factor (HGF) triggered its expression exclusively at the early-differentiation phase. In order to verify this concept, the present study was designed to clarify a paracrine source of HGF release. In vitro experiments demonstrated that activated anti-inflammatory macrophages (CD206-positive M2) produce HGF and thereby promote myoblast chemoattraction and Sema3A expression. Media from pro-inflammatory macrophage cultures (M1) did not show any significant effect. M2 also enhanced the expression of myoblast-differentiation markers in culture, and infiltrated predominantly at the early-differentiation phase (3-5 days post-injury); M2 were confirmed to produce HGF as monitored by in vivo/ex vivo immunocytochemistry of CD11b/CD206/HGF-positive cells and by HGF in situ hybridization of cardiotoxin- or crush-injured tibialis anterior muscle, respectively. These studies advance our understanding of the stage-specific activation of Sema3A expression signaling. Findings, therefore, encourage the idea that M2 contribute to spatiotemporal up-regulation of extracellular Sema3A concentrations by producing HGF that, in turn, stimulates a burst of Sema3A secretion by myoblasts that are recruited to site of injury. This model may ensure a coordinated delay in re-attachment of motoneuron terminals onto damaged fibers early in muscle regeneration, and thus synchronize the recovery of muscle-fiber integrity and the early resolution of inflammation after injury.

元の言語英語
ページ(範囲)272-285
ページ数14
ジャーナルInternational Journal of Biochemistry and Cell Biology
54
DOI
出版物ステータス出版済み - 1 1 2014

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Semaphorin-3A
Hepatocyte Growth Factor
Macrophages
Myoblasts
Muscle
Anti-Inflammatory Agents
Muscles
Wounds and Injuries
Skeletal Muscle Satellite Cells
Cardiotoxins
Fibers
Differentiation Antigens
Motor Neurons
Stem cells
Cell culture
In Situ Hybridization
Regeneration
Up-Regulation
Stem Cells
Chemical activation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cell Biology

これを引用

Implication of anti-inflammatory macrophages in regenerative moto-neuritogenesis : Promotion of myoblast migration and neural chemorepellent semaphorin 3A expression in injured muscle. / Sakaguchi, Shohei; Shono, Jun Ichi; Suzuki, Takahiro; Sawano, Shoko; Anderson, Judy E.; Do, Mai Khoi Q.; Ohtsubo, Hideaki; Mizunoya, Wataru; Sato, Yusuke; Nakamura, Mako; Furuse, Mitsuhiro; Yamada, Koji; Ikeuchi, Yoshihide; Tatsumi, Ryuichi.

:: International Journal of Biochemistry and Cell Biology, 巻 54, 01.01.2014, p. 272-285.

研究成果: ジャーナルへの寄稿記事

Sakaguchi, Shohei ; Shono, Jun Ichi ; Suzuki, Takahiro ; Sawano, Shoko ; Anderson, Judy E. ; Do, Mai Khoi Q. ; Ohtsubo, Hideaki ; Mizunoya, Wataru ; Sato, Yusuke ; Nakamura, Mako ; Furuse, Mitsuhiro ; Yamada, Koji ; Ikeuchi, Yoshihide ; Tatsumi, Ryuichi. / Implication of anti-inflammatory macrophages in regenerative moto-neuritogenesis : Promotion of myoblast migration and neural chemorepellent semaphorin 3A expression in injured muscle. :: International Journal of Biochemistry and Cell Biology. 2014 ; 巻 54. pp. 272-285.
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abstract = "Regenerative mechanisms that regulate intramuscular motor innervation are thought to reside in the spatiotemporal expression of axon-guidance molecules. Our previous studies proposed a heretofore unexplored role of resident myogenic stem cell (satellite cell)-derived myoblasts as a key presenter of a secreted neural chemorepellent semaphorin 3A (Sema3A); hepatocyte growth factor (HGF) triggered its expression exclusively at the early-differentiation phase. In order to verify this concept, the present study was designed to clarify a paracrine source of HGF release. In vitro experiments demonstrated that activated anti-inflammatory macrophages (CD206-positive M2) produce HGF and thereby promote myoblast chemoattraction and Sema3A expression. Media from pro-inflammatory macrophage cultures (M1) did not show any significant effect. M2 also enhanced the expression of myoblast-differentiation markers in culture, and infiltrated predominantly at the early-differentiation phase (3-5 days post-injury); M2 were confirmed to produce HGF as monitored by in vivo/ex vivo immunocytochemistry of CD11b/CD206/HGF-positive cells and by HGF in situ hybridization of cardiotoxin- or crush-injured tibialis anterior muscle, respectively. These studies advance our understanding of the stage-specific activation of Sema3A expression signaling. Findings, therefore, encourage the idea that M2 contribute to spatiotemporal up-regulation of extracellular Sema3A concentrations by producing HGF that, in turn, stimulates a burst of Sema3A secretion by myoblasts that are recruited to site of injury. This model may ensure a coordinated delay in re-attachment of motoneuron terminals onto damaged fibers early in muscle regeneration, and thus synchronize the recovery of muscle-fiber integrity and the early resolution of inflammation after injury.",
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AU - Sakaguchi, Shohei

AU - Shono, Jun Ichi

AU - Suzuki, Takahiro

AU - Sawano, Shoko

AU - Anderson, Judy E.

AU - Do, Mai Khoi Q.

AU - Ohtsubo, Hideaki

AU - Mizunoya, Wataru

AU - Sato, Yusuke

AU - Nakamura, Mako

AU - Furuse, Mitsuhiro

AU - Yamada, Koji

AU - Ikeuchi, Yoshihide

AU - Tatsumi, Ryuichi

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