SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration
SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-γ) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-γ-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-γ-induced cross-tolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2020 |
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Erschienen: |
2020 |
Enthalten in: |
Zur Gesamtaufnahme - volume:36 |
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Enthalten in: |
Neuroscience bulletin - 36(2020), 7 vom: 18. Juli, Seite 778-792 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Zhang, Xuejie [VerfasserIn] |
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Links: |
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Themen: |
82115-62-6 |
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Anmerkungen: |
Date Completed 19.07.2021 Date Revised 19.07.2021 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1007/s12264-020-00493-8 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM308910001 |
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520 | |a SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-γ) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-γ-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-γ-induced cross-tolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals | ||
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700 | 1 | |a Wang, Yingjie |e verfasserin |4 aut | |
700 | 1 | |a Zhou, Yue |e verfasserin |4 aut | |
700 | 1 | |a Wang, Wenjuan |e verfasserin |4 aut | |
700 | 1 | |a Song, Tiancheng |e verfasserin |4 aut | |
700 | 1 | |a Du, Nan |e verfasserin |4 aut | |
700 | 1 | |a Gu, Xingxing |e verfasserin |4 aut | |
700 | 1 | |a Luo, Yi |e verfasserin |4 aut | |
700 | 1 | |a Wang, Yongjun |e verfasserin |4 aut | |
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