Algesic MBP peptide induce pain-specific signaling in rodent Schwann Cells
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ABSTRACT:
PROVIDER: PRJNA418791 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6300250.fastq.gz | Fastqsanger.gz | |||
| SRR6300245.fastq.gz | Fastqsanger.gz | |||
| SRR6300246.fastq.gz | Fastqsanger.gz | |||
| SRR6300247.fastq.gz | Fastqsanger.gz | |||
| SRR6300248.fastq.gz | Fastqsanger.gz |
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Project description:We demonstrated the pain-specific response to the algesic peptide fragment MBP84-104 of myelin basic protein that induces pain if injected into sciatic nerve of rats and mice. We used the wild-type peptide MBP 84-104, H89G mutant peptide (MBP84-104-H89G), scramble peptide (MBP84-104-SCR) and phosphomimetic peptide MBP84-104-mimTT to stimulate the primary rat Schwann cell cultures. After 24h we isolated total RNA and conducted genome wide RNA-seq. In addition, we performed RNA-seq using Schwann cells constitutively expressing an MBP84-104-mCherry construct. The gene expression data was analyzed using Ingenuity Pathway Analysis software. We conclude that the Schwann cells expressing MBP84-104 constructs stimulate pain-specific signaling pathways thus representing a relevant model to study neuropathic pain.
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Project description:The aim of this study was to identify differently expressed genes between C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells. To elucidate the unresolved mechanism behind the promoting effect of C3156-181 on PNR we cultured primary rat neonatal SCs and treated them for up to 72 h with C3 or C3156-181. We then performed gene expression microarray analysis Results from two loops of two different treatment times are summarized in this study. The samples were taken from two C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cell cultures. Microarrays were hybridized in a loop approach. Results from two loops that map to two different sampling times (loop1: after 12 hours, loop2: after 72) are compared in this study. The data in this file represents loop1. The samples were taken from untreated, C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells.
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Project description:An insulating myelin sheath ensures saltatory conduction of mechanosensory A afferents. Myelin damage results in the electrical instability of A fibers and the ability to generate pain in response to light touch/pressure (mechanical allodynia). We have hypothesized and then established that the release of T cell epitopes of myelin basic protein (MBP) enables nociceptive circuitry in myelinated fibers. Thus, mass spectrometry analysis of the rat sciatic nerve proteome followed by bioinformatics examination of the datasets revealed a loss of MBP and activation of T-helper cell signaling in the nerves undergoing chronic constriction injury (CCI). Matrix metalloproteinase-9 (MMP-9) proteolysis resulted in the MBP digest peptides, including the MBP84-104 and MBP68-86 regions, which exhibit prominent immunogenic epitopes. Myelin-forming Schwann cells and paranodal areas accumulated MHCII, MMP-9 and the degraded MBP at the sciatic nerve injury site. Administration of the immunodominant MBP84-104 and MBP68-86 peptides but not of the control peptides in a naïve rat sciatic nerve produced robust mechanical allodynia. Allodynia was accompanied by the T cell infiltration and an increase in MHCII, IL-17A and TNF- levels at the nerve injection site and the segmental ganglia. The pro-nociceptive activity of the synthetic MBP84-104 diminished in athymic nude rats lacking T cells. SB-3CT, an antagonist of MMP-9, inhibited mechanical allodynia, neuroinflammation and spinal sensitization after CCI. Collectively, our novel data implicate, for the first time, MMP-mediated cleavage of MBP and the resulting MBP digest fragments as a major cause of neuropathic pain. Gene extression profiling of total RNAs extracted from rat sciatic nerves, dorsal root ganglion and spinal cords after MBP84-104 peptide injection
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Project description:There is an imminent need for safe and efficient chronic pain medications. Regulator of G-protein signaling 4 (RGS4) is a multi-functional signal transduction protein, widely expressed in the pain matrix. Here, we demonstrate that RGS4 plays a prominentrole in the maintenance of chronic pain symptoms in male and female mice. Using genetically modified mice, we show a dynamicrole of RGS4 in recovery from symptoms of sensory hypersensitivity deriving from hindpaw inflammation or hindlimb nerveinjury. We also demonstrate an important role of RGS4 actions in gene expression patterns induced by chronic pain states in themouse thalamus. Our findings provide novel insight into mechanisms associated with the maintenance of chronic pain states anddemonstrate that interventions in RGS4 activity promote recovery from sensory hypersensitivity symptoms.
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Project description:We focused on NR2F1 and NR2F2 (CoupTF1/CoupTF2) since they are expressed from neural crest through Schwann cell maturity, and found that knockdown of nuclear receptors Nr2f1 and Nr2f2 in primary Schwann cells downregulated genes such as Myelin Basic Protein (Mbp), Desert Hedgehog (Dhh), and N-Myc Downstream Regulated 1 (Ndrg1). In this study, we have elucidated a NR2F-regulated target gene network in Schwann cells, which revealed enrichment for non-myelinating Schwann cell genes. We used Cut&Run in S16 Schwann cells to show novel, genome-wide binding sites of NR2F1/2 and downstream transcription factors, YY1, SREBP1, Retinoid X Receptor (RXRG) and TEA-Domain factor (TEAD1). Our study elucidates the transcriptional cooperation that forms unique enhancer landscapes and the regulatory network that targets non-myelinating Schwann cells.
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Project description:The important contribution of glia to mechanisms of injury and repair of the nervous system is increasingly recognized. In stark contrast to the central nervous system (CNS), the peripheral nervous system (PNS) has a remarkable capacity for regeneration after injury. Schwann cells are recognized as key contributors to PNS regeneration but the molecular underpinnings of the Schwann cell response to injury remain incompletely understood. To gain insight into the acute SC injury response, we provide an RNAseq database of Schwann cells purified acutely from the naïve and injured rodent sciatic nerve at 3, 5, and 7 days post injury. Bioinformatic analysis provides validation of cell purity and dataset integrity as well as identification of discrete modules of genes that follow distinct patterns of regulation in the first days after injury and their corresponding molecular pathways. Our dataset provides a helpful resource for further deciphering the SC injury response and provides a depth of transcriptional data that can complement the findings of recent single cell sequencing approaches. In addition, as more data becomes available on the response of CNS glia to injury, we anticipate that this dataset will provide a valuable platform for understanding key differences in the PNS and CNS glial responses to injury and for designing approaches to ameliorate CNS regeneration.
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