Endogenous opioid signalling regulates spinal ependymal cell proliferation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1076908 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27983678_1.fastq.gz | Fastqsanger.gz | |||
| SRR27983678_2.fastq.gz | Fastqsanger.gz | |||
| SRR27983679_1.fastq.gz | Fastqsanger.gz | |||
| SRR27983679_2.fastq.gz | Fastqsanger.gz | |||
| SRR27983680_1.fastq.gz | Fastqsanger.gz |
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Project description:After injury, mammalian spinal cords develop scars to confine the lesion and prevent further damage. However, excessive scarring can hinder neural regeneration and functional recovery. These competing actions underscore the importance of developing therapeutic strategies to dynamically modulate scar progression. Previous research on scarring has primarily focused on astrocytes, but recent evidence has suggested that ependymal cells also participate. Ependymal cells normally form the epithelial layer encasing the central canal, but they undergo massive proliferation and differentiation into astroglia following certain injuries, becoming a core scar component. However, the mechanisms regulating ependymal proliferation in vivo remain unclear. Here we uncover an endogenous κ-opioid signalling pathway that controls ependymal proliferation. Specifically, we detect expression of the κ-opioid receptor, OPRK1, in a functionally under-characterized cell type known as cerebrospinal fluid-contacting neuron (CSF-cN). We also discover a neighbouring cell population that expresses the cognate ligand prodynorphin (PDYN). Whereas κ-opioids are typically considered inhibitory, they excite CSF-cNs to inhibit ependymal proliferation. Systemic administration of a κ-antagonist enhances ependymal proliferation in uninjured spinal cords in a CSF-cN-dependent manner. Moreover, a κ-agonist impairs ependymal proliferation, scar formation and motor function following injury. Together, our data suggest a paracrine signalling pathway in which PDYN+ cells tonically release κ-opioids to stimulate CSF-cNs and suppress ependymal proliferation, revealing an endogenous mechanism and potential pharmacological strategy for modulating scarring after spinal cord injury.
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Project description:The spinal cord neural stem cell potential is contained within the ependymal cells lining the central canal. Ependymal cells are, however, heterogeneous and we know little about what this reflects. To gain new insights into ependymal cell heterogeneity, we microdissected the ependymal cell layer from the thoracic spinal cord of 4 FOXJ1-EGFP transgenic mice (2.5-to-3-month old). After after dissociating the tissue into a cell suspension, we sorted single GFP-positive ependymal cells into lysis plates. cDNA synthesis was performed using Smart-seq2 technology.
2022-12-13 | E-MTAB-11563 | biostudies-arrayexpress
Project description:In contrast to ependymal cells in the lateral ventricle wall (LVW), spinal cord (SC) ependymal cells possess certain neural stem cell characteristics. Isolated CD133+/CD24+/CD45-/CD34- ependymal cells from the SC displayed in vitro self renewal and differentiation capacity, whereas those from the LVW did not. The molecular basis of this difference is unknown. In this study, antibodies against multiple surface markers were applied to isolate SC and LVW ependymal cells which allowed a direct comparison of their in vitro behavior and gene expression profile. cRNA samples of three independent biological replicates of CD133+/CD24+/CD45-/CD34- LVW ependymal cells, CD133+/CD24+/CD45-/CD34- SC ependymal cells, CD133+/CD24-/CD45-/CD34- radial glial cells, and SC ependymal cell-derived NSPs were hybridized onto Illumina MouseWG-6 v1.1 gene expression arrays
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Project description:After spinal cord injury, ependymal cells considered as stem cells activate, proliferate and differentiate mainly into glial cells. To understand this further at the molecular level, we performed RNA profiling of these cells in situ using laser-dissection and also when they are cultured as neurospheres in different conditions (growth, differentiation, dedifferentiation) Abstract: Numerous vertebrates, including Human, maintain a pool of immature cells in the ependymal region of the adult spinal cord. During injury, these ependymal cells, considered as multipotent stem cells, rapidly activate, proliferate and generate neurons and glial cells in lower vertebrates or mainly glial cells in mammals. The mechanisms underlying this activation are ill-defined and we intended to fill this gap by performing RNA profiling of mouse ependymal region after lesion. Bioinformatics and immunofluorescence identified activation of STAT3 and ERK/MAPK signaling in ependymal cells after injury. This was also accompanied by downregulation of cilia-associated genes and FoxJ1, a central transcription factor of ciliogenesis. Six genes were upregulated more than 20 fold, namely Crym, Ecm1, Ifi202b, Nupr1, Osmr, Rbp1, Thbs2 whereas only one, Acta1 was downregulated to this extent. We explored further the role and regulation in ependymal cells of Osmr, the receptor for oncostatin (OSM). This inflammatory cytokine is specifically expressed by microglia cells and we observed interactions between these cells and ependymal cells in vivo. Using culture of ependymal cells in neurospheres, we found that several cytokines induced OSMR, OSM being the most potent. OSMR is also upregulated by co-culture with OSM-expressing microglial cells. Treatment of spinal cord neural stem cells with OSM decreased their proliferation, upregulate p-Stat3 and reduced their differentiation into oligodendrocyte-lineage Olig1+ cells. These results suggest an important role for microglia-derived oncostatin in the activation and fate of spinal cord ependymal cell.
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Project description:We performed single cell RNA sequencing to examine the reaction of a subpopulation of ependymal cells, EpA cells, to spinal cord injury. The experiment contains cells from spinal cords of Troy-CreERT2 mice on a Rosa26-tdTomato background. The spinal cord samples come from uninjured and injured spinal cords (3 days after injury).
2022-01-03 | GSE192824 | GEO
Project description:The adult spinal cord contains a population of ependymal-derived neural stem/progenitor cells (epNSPCs) that are normally quiescent, but are activated to proliferate, differentiate, and migrate after spinal cord injury. The mechanisms that regulate their response to injury cues, however, remain unknown. Here, we demonstrate that excitotoxic levels of glutamate promote the proliferation and astrocytic fate specification of adult spinal cord epNSPCs through CP-AMPAR signaling.
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Project description:Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, which shows that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene, Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis after spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals. Spinal cord injury or control sham injury was performed on adult zebrafish. After 4, 12, or 264 hrs, a 5 mm segment of spinal cord was dissected and processed (as a pool from 5 animals) in three replicate groups for each time point and treatment.
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Project description:Adult zebrafish have the ability to recover from spinal cord injury and exhibit re-growth of descending axons from the brainstem to the spinal cord. We performed gene expression analysis using microarray to find damage-induced genes after spinal cord injury, which shows that Sox11b mRNA is up-regulated at 11 days after injury. However, the functional relevance of Sox11b for regeneration is not known. Here, we report that the up-regulation of Sox11b mRNA after spinal cord injury is mainly localized in ependymal cells lining the central canal and in newly differentiating neuronal precursors or immature neurons. Using an in vivo morpholino-based gene knockout approach, we demonstrate that Sox11b is essential for locomotor recovery after spinal cord injury. In the injured spinal cord, expression of the neural stem cell associated gene, Nestin, and the proneural gene Ascl1a (Mash1a), which are involved in the self-renewal and cell fate specification of endogenous neural stem cells, respectively, is regulated by Sox11b. Our data indicate that Sox11b promotes neuronal determination of endogenous stem cells and regenerative neurogenesis after spinal cord injury in the adult zebrafish. Enhancing Sox11b expression to promote proliferation and neurogenic determination of endogenous neural stem cells after injury may be a promising strategy in restorative therapy after spinal cord injury in mammals.
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Project description:NSCs adhesion affinity along the AP axis is under the control of endogenous signalling molecular networks, the Wnt and RA signalling The caudal spinal cord domain expresses a high amount of ECM genes compare to rostral.
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