Transmembrane proteoglycans syndecan-2, 4, receptor candidates for the impact of HGF and FGF2 on semaphorin 3A expression in early-differentiated myoblasts

Mai Khoi Q. Do, Naomi Shimizu, Takahiro Suzuki, Hideaki Ohtsubo, Wataru Mizunoya, Mako Nakamura, Shoko Sawano, Mitsuhiro Furuse, Yoshihide Ikeuchi, Judy E. Anderson, Ryuichi Tatsumi

研究成果: ジャーナルへの寄稿記事

4 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 an 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) and basic fibroblast growth factor (FGF2) triggered its expression exclusively at the early differentiation phase. In order to advance this concept, the present study described that transmembrane heparan/chondroitin sulfate proteoglycans syndecan-2, 4 may be the plausible receptor candidates for HGF and FGF2 to signal Sema3A expression. Results showed that mRNA expression of syndecan-2, 4 was abundant (two magnitudes higher than syndecan-1, 3) in early-differentiated myoblasts and their in vitro knockdown diminished the HGF/FGF2-induced expression of Sema3A down to a baseline level. Pretreatment with heparitinase and chondroitinase ABC decreased the HGF and FGF2 responses, respectively, in non-knockdown cultures, supporting a possible model that HGF and FGF2 may bind to heparan and chondroitin sulfate chains of syndecan-2, 4 to signal Sema3A expression. The findings, therefore, extend our understanding that HGF/FGF2-syndecan-2, 4 association may stimulate a burst of Sema3A secretion by myoblasts recruited to the site of muscle injury; this would ensure a coordinated delay in the attachment of motoneuron terminals onto fibers early in muscle regeneration, and thus synchronize the recovery of muscle fiber integrity and the early resolution of inflammation after injury with reinnervation toward functional recovery.

元の言語英語
記事番号e12553
ジャーナルPhysiological Reports
3
発行部数9
DOI
出版物ステータス出版済み - 1 1 2015

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Syndecan-2
Syndecan-4
Semaphorin-3A
Hepatocyte Growth Factor
Myoblasts
Fibroblast Growth Factor 2
Proteoglycans
heparitinsulfate lyase
Muscles
Syndecan-3
Skeletal Muscle Satellite Cells
Syndecan-1
Chondroitin ABC Lyase
Proto-Oncogene Proteins c-met
Chondroitin Sulfate Proteoglycans
Heparan Sulfate Proteoglycans
Heparitin Sulfate
Chondroitin Sulfates
Wounds and Injuries
Motor Neurons

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

これを引用

Transmembrane proteoglycans syndecan-2, 4, receptor candidates for the impact of HGF and FGF2 on semaphorin 3A expression in early-differentiated myoblasts. / Do, Mai Khoi Q.; Shimizu, Naomi; Suzuki, Takahiro; Ohtsubo, Hideaki; Mizunoya, Wataru; Nakamura, Mako; Sawano, Shoko; Furuse, Mitsuhiro; Ikeuchi, Yoshihide; Anderson, Judy E.; Tatsumi, Ryuichi.

:: Physiological Reports, 巻 3, 番号 9, e12553, 01.01.2015.

研究成果: ジャーナルへの寄稿記事

Do, Mai Khoi Q. ; Shimizu, Naomi ; Suzuki, Takahiro ; Ohtsubo, Hideaki ; Mizunoya, Wataru ; Nakamura, Mako ; Sawano, Shoko ; Furuse, Mitsuhiro ; Ikeuchi, Yoshihide ; Anderson, Judy E. ; Tatsumi, Ryuichi. / Transmembrane proteoglycans syndecan-2, 4, receptor candidates for the impact of HGF and FGF2 on semaphorin 3A expression in early-differentiated myoblasts. :: Physiological Reports. 2015 ; 巻 3, 番号 9.
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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 an 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) and basic fibroblast growth factor (FGF2) triggered its expression exclusively at the early differentiation phase. In order to advance this concept, the present study described that transmembrane heparan/chondroitin sulfate proteoglycans syndecan-2, 4 may be the plausible receptor candidates for HGF and FGF2 to signal Sema3A expression. Results showed that mRNA expression of syndecan-2, 4 was abundant (two magnitudes higher than syndecan-1, 3) in early-differentiated myoblasts and their in vitro knockdown diminished the HGF/FGF2-induced expression of Sema3A down to a baseline level. Pretreatment with heparitinase and chondroitinase ABC decreased the HGF and FGF2 responses, respectively, in non-knockdown cultures, supporting a possible model that HGF and FGF2 may bind to heparan and chondroitin sulfate chains of syndecan-2, 4 to signal Sema3A expression. The findings, therefore, extend our understanding that HGF/FGF2-syndecan-2, 4 association may stimulate a burst of Sema3A secretion by myoblasts recruited to the site of muscle injury; this would ensure a coordinated delay in the attachment of motoneuron terminals onto fibers early in muscle regeneration, and thus synchronize the recovery of muscle fiber integrity and the early resolution of inflammation after injury with reinnervation toward functional recovery.",
author = "Do, {Mai Khoi Q.} and Naomi Shimizu and Takahiro Suzuki and Hideaki Ohtsubo and Wataru Mizunoya and Mako Nakamura and Shoko Sawano and Mitsuhiro Furuse and Yoshihide Ikeuchi and Anderson, {Judy E.} and Ryuichi Tatsumi",
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AU - Do, Mai Khoi Q.

AU - Shimizu, Naomi

AU - Suzuki, Takahiro

AU - Ohtsubo, Hideaki

AU - Mizunoya, Wataru

AU - Nakamura, Mako

AU - Sawano, Shoko

AU - Furuse, Mitsuhiro

AU - Ikeuchi, Yoshihide

AU - Anderson, Judy E.

AU - Tatsumi, Ryuichi

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Y1 - 2015/1/1

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