期刊
SCIENTIFIC REPORTS
卷 8, 期 -, 页码 -出版社
NATURE RESEARCH
DOI: 10.1038/s41598-017-18757-1
关键词
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资金
- National Institutes of Health [R03NS078519, R01GM104123, R01NS078165]
- Feinstein Institute for Medical Research
- Marine Biological Laboratory
- Charles Evans Foundation Research Award
- Albert and Ellen Grass Foundation Faculty Research Award
- Eugene and Millicent Bell Fellowship Fund in Tissue Engineering
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM104123] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS078165, R03NS078519] Funding Source: NIH RePORTER
In mammals, spinal cord injury (SCI) leads to dramatic losses in neurons and synaptic connections, and consequently function. Unlike mammals, lampreys are vertebrates that undergo spontaneous regeneration and achieve functional recovery after SCI. Therefore our goal was to determine the complete transcriptional responses that occur after SCI in lampreys and to identify deeply conserved pathways that promote regeneration. We performed RNA-Seq on lamprey spinal cord and brain throughout the course of functional recovery. We describe complex transcriptional responses in the injured spinal cord, and somewhat surprisingly, also in the brain. Transcriptional responses to SCI in lampreys included transcription factor networks that promote peripheral nerve regeneration in mammals such as Atf3 and Jun. Furthermore, a number of highly conserved axon guidance, extracellular matrix, and proliferation genes were also differentially expressed after SCI in lampreys. Strikingly, similar to 3% of differentially expressed transcripts belonged to the Wnt pathways. These included members of the Wnt and Frizzled gene families, and genes involved in downstream signaling. Pharmacological inhibition of Wnt signaling inhibited functional recovery, confirming a critical role for this pathway. These data indicate that molecular signals present in mammals are also involved in regeneration in lampreys, supporting translational relevance of the model.
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