GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury

Xian Huang, Jin Mo Kim, Tae Ho Kong, So Ra Park, Yoon Ha, Moon Hang Kim, Hyeonseon Park, Seung Hwan Yoon, Hyung Chun Park, Jong Oon Park, Byoung Hyun Min, Byung Hyune Choi

Research output: Contribution to journalArticle

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Abstract

Object: This study investigated the effects of granulocyte macrophage-colony stimulating factor (GM-CSF) on the scar formation and repair of spinal cord tissues in rat spinal cord injury (SCI) model. Methods: Sprague-Dawley male rats (8 weeks old) were randomly divided into the sham-operated group, spinal cord injury group, and injury with GM-CSF treated group. A spinal cord injury was induced at T9/10 levels of rat spinal cord using a vascular clip. GM-CSF was administrated via intraperitoneal (IP) injection or on the dural surface using Gelfoam at the time of SCI. The morphological changes, tissue integrity, and scar formation were evaluated until 4 weeks after SCI using histological and immunohistochemical analyses. Results: The administration of GM-CSF either via IP injection or local treatment significantly reduced the cavity size and glial scar formation at 3-4 weeks after SCI. GM-CSF also reduced the expression of core proteins of chondroitin sulfate proteoglycans (CSPGs) such as neurocan and NG2 but not phosphacan. In particular, an intensive expression of glial fibriallary acidic protein (GFAP) and neurocan found around the cavity at 4 weeks was obviously suppressed by GM-CSF. Immunostaining for neurofilament (NF) and Luxol fast blue (LFB) showed that GM-CSF preserved well the axonal arrangement and myelin structure after SCI. The expression of GAP-43, a marker of regenerating axons, also apparently increased in the rostral grey matter by GM-CSF. Conclusion: These results suggest that GM-CSF could enhance long-term recovery from SCI by suppressing the glial scar formation and enhancing the integrity of axonal structure.

Original languageEnglish
Pages (from-to)87-97
Number of pages11
JournalJournal of the Neurological Sciences
Volume277
Issue number1-2
DOIs
Publication statusPublished - 2009 Feb 15

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Granulocyte-Macrophage Colony-Stimulating Factor
Spinal Cord Injuries
Neuroglia
Cicatrix
Neurocan
Intraperitoneal Injections
Class 5 Receptor-Like Protein Tyrosine Phosphatases
Spinal Cord Regeneration
Absorbable Gelatin Sponge
GAP-43 Protein
Chondroitin Sulfate Proteoglycans
Intermediate Filaments
Myelin Sheath
Surgical Instruments
Blood Vessels
Sprague Dawley Rats
Axons
Spinal Cord
Proteins
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

Huang, Xian ; Kim, Jin Mo ; Kong, Tae Ho ; Park, So Ra ; Ha, Yoon ; Kim, Moon Hang ; Park, Hyeonseon ; Yoon, Seung Hwan ; Park, Hyung Chun ; Park, Jong Oon ; Min, Byoung Hyun ; Choi, Byung Hyune. / GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury. In: Journal of the Neurological Sciences. 2009 ; Vol. 277, No. 1-2. pp. 87-97.
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abstract = "Object: This study investigated the effects of granulocyte macrophage-colony stimulating factor (GM-CSF) on the scar formation and repair of spinal cord tissues in rat spinal cord injury (SCI) model. Methods: Sprague-Dawley male rats (8 weeks old) were randomly divided into the sham-operated group, spinal cord injury group, and injury with GM-CSF treated group. A spinal cord injury was induced at T9/10 levels of rat spinal cord using a vascular clip. GM-CSF was administrated via intraperitoneal (IP) injection or on the dural surface using Gelfoam at the time of SCI. The morphological changes, tissue integrity, and scar formation were evaluated until 4 weeks after SCI using histological and immunohistochemical analyses. Results: The administration of GM-CSF either via IP injection or local treatment significantly reduced the cavity size and glial scar formation at 3-4 weeks after SCI. GM-CSF also reduced the expression of core proteins of chondroitin sulfate proteoglycans (CSPGs) such as neurocan and NG2 but not phosphacan. In particular, an intensive expression of glial fibriallary acidic protein (GFAP) and neurocan found around the cavity at 4 weeks was obviously suppressed by GM-CSF. Immunostaining for neurofilament (NF) and Luxol fast blue (LFB) showed that GM-CSF preserved well the axonal arrangement and myelin structure after SCI. The expression of GAP-43, a marker of regenerating axons, also apparently increased in the rostral grey matter by GM-CSF. Conclusion: These results suggest that GM-CSF could enhance long-term recovery from SCI by suppressing the glial scar formation and enhancing the integrity of axonal structure.",
author = "Xian Huang and Kim, {Jin Mo} and Kong, {Tae Ho} and Park, {So Ra} and Yoon Ha and Kim, {Moon Hang} and Hyeonseon Park and Yoon, {Seung Hwan} and Park, {Hyung Chun} and Park, {Jong Oon} and Min, {Byoung Hyun} and Choi, {Byung Hyune}",
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Huang, X, Kim, JM, Kong, TH, Park, SR, Ha, Y, Kim, MH, Park, H, Yoon, SH, Park, HC, Park, JO, Min, BH & Choi, BH 2009, 'GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury', Journal of the Neurological Sciences, vol. 277, no. 1-2, pp. 87-97. https://doi.org/10.1016/j.jns.2008.10.022

GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury. / Huang, Xian; Kim, Jin Mo; Kong, Tae Ho; Park, So Ra; Ha, Yoon; Kim, Moon Hang; Park, Hyeonseon; Yoon, Seung Hwan; Park, Hyung Chun; Park, Jong Oon; Min, Byoung Hyun; Choi, Byung Hyune.

In: Journal of the Neurological Sciences, Vol. 277, No. 1-2, 15.02.2009, p. 87-97.

Research output: Contribution to journalArticle

TY - JOUR

T1 - GM-CSF inhibits glial scar formation and shows long-term protective effect after spinal cord injury

AU - Huang, Xian

AU - Kim, Jin Mo

AU - Kong, Tae Ho

AU - Park, So Ra

AU - Ha, Yoon

AU - Kim, Moon Hang

AU - Park, Hyeonseon

AU - Yoon, Seung Hwan

AU - Park, Hyung Chun

AU - Park, Jong Oon

AU - Min, Byoung Hyun

AU - Choi, Byung Hyune

PY - 2009/2/15

Y1 - 2009/2/15

N2 - Object: This study investigated the effects of granulocyte macrophage-colony stimulating factor (GM-CSF) on the scar formation and repair of spinal cord tissues in rat spinal cord injury (SCI) model. Methods: Sprague-Dawley male rats (8 weeks old) were randomly divided into the sham-operated group, spinal cord injury group, and injury with GM-CSF treated group. A spinal cord injury was induced at T9/10 levels of rat spinal cord using a vascular clip. GM-CSF was administrated via intraperitoneal (IP) injection or on the dural surface using Gelfoam at the time of SCI. The morphological changes, tissue integrity, and scar formation were evaluated until 4 weeks after SCI using histological and immunohistochemical analyses. Results: The administration of GM-CSF either via IP injection or local treatment significantly reduced the cavity size and glial scar formation at 3-4 weeks after SCI. GM-CSF also reduced the expression of core proteins of chondroitin sulfate proteoglycans (CSPGs) such as neurocan and NG2 but not phosphacan. In particular, an intensive expression of glial fibriallary acidic protein (GFAP) and neurocan found around the cavity at 4 weeks was obviously suppressed by GM-CSF. Immunostaining for neurofilament (NF) and Luxol fast blue (LFB) showed that GM-CSF preserved well the axonal arrangement and myelin structure after SCI. The expression of GAP-43, a marker of regenerating axons, also apparently increased in the rostral grey matter by GM-CSF. Conclusion: These results suggest that GM-CSF could enhance long-term recovery from SCI by suppressing the glial scar formation and enhancing the integrity of axonal structure.

AB - Object: This study investigated the effects of granulocyte macrophage-colony stimulating factor (GM-CSF) on the scar formation and repair of spinal cord tissues in rat spinal cord injury (SCI) model. Methods: Sprague-Dawley male rats (8 weeks old) were randomly divided into the sham-operated group, spinal cord injury group, and injury with GM-CSF treated group. A spinal cord injury was induced at T9/10 levels of rat spinal cord using a vascular clip. GM-CSF was administrated via intraperitoneal (IP) injection or on the dural surface using Gelfoam at the time of SCI. The morphological changes, tissue integrity, and scar formation were evaluated until 4 weeks after SCI using histological and immunohistochemical analyses. Results: The administration of GM-CSF either via IP injection or local treatment significantly reduced the cavity size and glial scar formation at 3-4 weeks after SCI. GM-CSF also reduced the expression of core proteins of chondroitin sulfate proteoglycans (CSPGs) such as neurocan and NG2 but not phosphacan. In particular, an intensive expression of glial fibriallary acidic protein (GFAP) and neurocan found around the cavity at 4 weeks was obviously suppressed by GM-CSF. Immunostaining for neurofilament (NF) and Luxol fast blue (LFB) showed that GM-CSF preserved well the axonal arrangement and myelin structure after SCI. The expression of GAP-43, a marker of regenerating axons, also apparently increased in the rostral grey matter by GM-CSF. Conclusion: These results suggest that GM-CSF could enhance long-term recovery from SCI by suppressing the glial scar formation and enhancing the integrity of axonal structure.

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