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- Okada Seiji
- SSP stem cell Unit, Kyushu University School of Medicine Department of Orthopaedic Surgery, Kyushu University School of Medicine
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- Nakamura Masaya
- Department of Orthopaedic Surgery, Keio University School of Medicine
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- Saiwai Hirokazu
- SSP stem cell Unit, Kyushu University School of Medicine Department of Orthopaedic Surgery, Kyushu University School of Medicine
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- Kumamaru Hiromi
- SSP stem cell Unit, Kyushu University School of Medicine Department of Orthopaedic Surgery, Kyushu University School of Medicine
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- Toyama Yoshiaki
- Department of Orthopaedic Surgery, Keio University School of Medicine
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- Iwamoto Yukihide
- Department of Orthopaedic Surgery, Kyushu University School of Medicine
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- Okano Hideyuki
- Department of Physiology, Keio University School of Medicine
この論文をさがす
抄録
In the injured central nervous system (CNS), reactive astrocytes form a glial scar and they are considered a physical barrier to prevent axonal regeneration by producing axonal growth inhibitors, such as chondroitin sulfate proteoglycans. However, the physiological role of reactive astrocytes remains to be elucidated. In this review, we showed that reactive astrocytes play a crucial role in wound healing and functional recovery. At the subacute phase of spinal cord injury (SCI), reactive astrocytes eventually migrated to the lesion epicenter and gradually compacted the infiltrated inflammatory cells and contracted the lesion area, and functional recovery was observed only in this repair phase. Selective deletion of the signal transducer and activator of transcription-3 (STAT3) in reactive astrocytes resulted in their limited migration associated with zinc signaling, markedly widespread damaged area and severe motor deficits. These results suggest that STAT3 is a key regulator of reactive astrocytes migration in the healing process after SCI, providing a beneficial aspect of reactive astrocytes after CNS injury.
収録刊行物
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- Inflammation and Regeneration
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Inflammation and Regeneration 29 (1), 35-39, 2009
一般社団法人 日本炎症・再生医学会
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詳細情報 詳細情報について
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- CRID
- 1390001205256255104
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- NII論文ID
- 130004482233
- 10024797022
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- NII書誌ID
- AA11508953
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- ISSN
- 18808190
- 18809693
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- NDL書誌ID
- 10173627
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可