原创力文档reactive astrocytes in glial scar attract olfactory ensheathing cells migration by secreted tnf-α in spinal cord lesion of rat反应性星形胶质细胞胶质疤痕吸引嗅鞘细胞移植的分泌tnf-α鼠的脊髓损伤.pdfVIP
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reactive astrocytes in glial scar attract olfactory ensheathing cells migration by secreted tnf-α in spinal cord lesion of rat反应性星形胶质细胞胶质疤痕吸引嗅鞘细胞移植的分泌tnf-α鼠的脊髓损伤
Reactive Astrocytes in Glial Scar Attract Olfactory
Ensheathing Cells Migration by Secreted TNF-a in Spinal
Cord Lesion of Rat
Zhida Su, Yimin Yuan, Jingjing Chen, Li Cao, Yanling Zhu, Liang Gao, Yang Qiu, Cheng He*
Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Minister of Education, Neuroscience Research Center of Changzheng Hospital, Second Military
Medical University, Shanghai, China
Abstract
Background: After spinal cord injury (SCI), the formation of glial scar contributes to the failure of injured adult axons to
regenerate past the lesion. Increasing evidence indicates that olfactory ensheathing cells (OECs) implanted into spinal cord
are found to migrate into the lesion site and induce axons regeneration beyond glial scar and resumption of functions.
However, little is known about the mechanisms of OECs migrating from injection site to glial scar/lesion site.
Methods and Findings: In the present study, we identified a link between OECs migration and reactive astrocytes in glial
scar that was mediated by the tumor necrosis factor-a (TNF-a). Initially, the Boyden chamber migration assay showed that
both glial scar tissue and reactive astrocyte-conditioned medium promoted OECs migration in vitro. Reactive astrocyte-
derived TNF-a and its type 1 receptor TNFR1 expressed on OECs were identified to be responsible for the promoting effect
on OECs migration. TNF-a-induced OECs migration was demonstrated depending on activation of the extracellular signal-
regulated kinase (ERK) signaling cascades. Furthermore, TNF-a secreted by reactive astrocytes in glial scar was also showed
to attract OECs migration in a spinal cord hemisection injury model of rat.
Conclusions: These findings showed that TNF-a was released by reactive astrocytes in glial scar and attracted OECs
migration by interacting with TNFR1 expressed on OECs v
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