Growth factor regulation of neural chemorepellent sema3A expression in satellite cell cultures

Q. do Mai-Khoi, Yusuke Sato, Naomi Shimizu, Takahiro Suzuki, Jun Ichi Shono, Wataru Mizunoya, Mako Nakamura, Yoshihide Ikeuchi, Judy E. Anderson, Ryuichi Tatsumi

研究成果: ジャーナルへの寄稿記事

24 引用 (Scopus)

抄録

Successful regeneration and remodeling of the intramuscular motoneuron network and neuromuscular connections are critical for restoring skeletal muscle function and physiological properties. The regulatory signals of such coordination remain unclear, although axon-guidance molecules may be involved. Recently, satellite cells, resident myogenic stem cells positioned beneath the basal lamina and at high density at the myoneural junction regions of mature fibers, were shown to upregulate a secreted neural chemorepellent semaphoring 3A (Sema3A) in response to in vivo muscle-crush injury. The initial report on that expression centered on the observation that hepatocyte growth factor (HGF), an essential cue in muscle fiber growth and regeneration, remarkably upregulates Sema3A expression in early differentiated satellite cells in vitro [Tatsumi et al., Am J Physiol Cell Physiol 297: C238-C252, 2009]. Here, we address regulatory effects of basic fibroblast growth factor (FGF2) and transforming growth factor (TGF)-βs on Sema3A expression in satellite cell cultures. When treated with FGF2, Sema3A message and protein were upregulated as revealed by reverse transcription-polymerase chain reaction and immunochemical studies. Sema3A upregulation by FGF2 was dose dependent with a maximum (8- to 1-fold relative to the control) at 2.5 ng/ml (150 pM) and occurred exclusively at the early differentiation stage. The response was highly comparable in dose response and timing to effects of HGF treatment, without any additive or synergistic effect from treatment with a combination of both potent upregulators. In contrast, TGF-β2 and -β3 potently decreased basal Sema3A expression; the maximum effect was at very low concentrations (40 and 8 pM, respectively) and completely cancelled the activities of FGF2 and HGF to upregulate Sema3A. These results therefore encourage the prospect that a time-coordinated increase in HGF, FGF2, and TGF-β ligands and their receptors promotes a programmed strategy for Sema3A expression that guarantees successful intramuscular motor reinnervation by delaying sprouting and reattachment of motoneuron terminals onto damaged muscle fibers early in regeneration pending restoration of muscle fiber contractile integrity.

元の言語英語
ジャーナルAmerican Journal of Physiology - Cell Physiology
301
発行部数5
DOI
出版物ステータス出版済み - 11 1 2011

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Semaphorin-3A
Fibroblast Growth Factor 2
Intercellular Signaling Peptides and Proteins
Hepatocyte Growth Factor
Cell Culture Techniques
Transforming Growth Factors
Up-Regulation
Regeneration
Muscles
Motor Neurons
Skeletal Muscle Satellite Cells
Neuromuscular Junction
Basement Membrane
Reverse Transcription
Cues
Skeletal Muscle
Stem Cells
Ligands
Polymerase Chain Reaction
Growth

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cell Biology

これを引用

Growth factor regulation of neural chemorepellent sema3A expression in satellite cell cultures. / do Mai-Khoi, Q.; Sato, Yusuke; Shimizu, Naomi; Suzuki, Takahiro; Shono, Jun Ichi; Mizunoya, Wataru; Nakamura, Mako; Ikeuchi, Yoshihide; Anderson, Judy E.; Tatsumi, Ryuichi.

:: American Journal of Physiology - Cell Physiology, 巻 301, 番号 5, 01.11.2011.

研究成果: ジャーナルへの寄稿記事

do Mai-Khoi, Q. ; Sato, Yusuke ; Shimizu, Naomi ; Suzuki, Takahiro ; Shono, Jun Ichi ; Mizunoya, Wataru ; Nakamura, Mako ; Ikeuchi, Yoshihide ; Anderson, Judy E. ; Tatsumi, Ryuichi. / Growth factor regulation of neural chemorepellent sema3A expression in satellite cell cultures. :: American Journal of Physiology - Cell Physiology. 2011 ; 巻 301, 番号 5.
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abstract = "Successful regeneration and remodeling of the intramuscular motoneuron network and neuromuscular connections are critical for restoring skeletal muscle function and physiological properties. The regulatory signals of such coordination remain unclear, although axon-guidance molecules may be involved. Recently, satellite cells, resident myogenic stem cells positioned beneath the basal lamina and at high density at the myoneural junction regions of mature fibers, were shown to upregulate a secreted neural chemorepellent semaphoring 3A (Sema3A) in response to in vivo muscle-crush injury. The initial report on that expression centered on the observation that hepatocyte growth factor (HGF), an essential cue in muscle fiber growth and regeneration, remarkably upregulates Sema3A expression in early differentiated satellite cells in vitro [Tatsumi et al., Am J Physiol Cell Physiol 297: C238-C252, 2009]. Here, we address regulatory effects of basic fibroblast growth factor (FGF2) and transforming growth factor (TGF)-βs on Sema3A expression in satellite cell cultures. When treated with FGF2, Sema3A message and protein were upregulated as revealed by reverse transcription-polymerase chain reaction and immunochemical studies. Sema3A upregulation by FGF2 was dose dependent with a maximum (8- to 1-fold relative to the control) at 2.5 ng/ml (150 pM) and occurred exclusively at the early differentiation stage. The response was highly comparable in dose response and timing to effects of HGF treatment, without any additive or synergistic effect from treatment with a combination of both potent upregulators. In contrast, TGF-β2 and -β3 potently decreased basal Sema3A expression; the maximum effect was at very low concentrations (40 and 8 pM, respectively) and completely cancelled the activities of FGF2 and HGF to upregulate Sema3A. These results therefore encourage the prospect that a time-coordinated increase in HGF, FGF2, and TGF-β ligands and their receptors promotes a programmed strategy for Sema3A expression that guarantees successful intramuscular motor reinnervation by delaying sprouting and reattachment of motoneuron terminals onto damaged muscle fibers early in regeneration pending restoration of muscle fiber contractile integrity.",
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AU - Suzuki, Takahiro

AU - Shono, Jun Ichi

AU - Mizunoya, Wataru

AU - Nakamura, Mako

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AU - Anderson, Judy E.

AU - Tatsumi, Ryuichi

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