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Expression data from periplaque regions in multiple sclerosis spinal cord

ABSTRACT: There have been few studies that have focused on the periplaque regions surrounding demyelinated plaques, especially in spinal cords. Areas of incomplete demyelination have been demonstrated but poorly studied. The present study aimed to analyze the molecular immunopathology of periplaque demyelinated lesions (PDLs) in the spinal cord of patients with secondary progressive multiple sclerosis (MS). To achieve this goal, the transcriptomic profiles of PDLs were analyzed in post-mortem tissues derived from the cervical spinal cord of 8 patients with primary or secondary progressive MS. Sixteen spinal cord samples were microdissected for RNA extraction and hybridization on Affymetrix microarrays. Eight periplaque samples (P) were compared to normal appearing white matter (N) from the same patient.

ORGANISM(S): Homo sapiens

SUBMITTER: Serge Nataf

PROVIDER: E-GEOD-52139 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from periplaque regions in multiple sclerosis spinal cord

Project description:There have been few studies that have focused on the periplaque regions surrounding demyelinated plaques, especially in spinal cords. Areas of incomplete demyelination have been demonstrated but poorly studied. The present study aimed to analyze the molecular immunopathology of periplaque demyelinated lesions (PDLs) in the spinal cord of patients with secondary progressive multiple sclerosis (MS). To achieve this goal, the transcriptomic profiles of PDLs were analyzed in post-mortem tissues derived from the cervical spinal cord of 8 patients with primary or secondary progressive MS.

2014-05-30 | GSE52139 | GEO

Danio spinal cord injury

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.

2010-10-19 | E-GEOD-20460 | biostudies-arrayexpress

Inhibition of spinal cord Hsp90 enhances morphine anti-nociception by activating an ERK/RSK pathway

Project description:Morphine and other opioids continue to be commonly utilized as clinical analgesics, despite their numerous adverse side effects, including respiratory depression, addiction, and tolerance. The modulation of µ-opioid receptor (MOR) signaling and subsequent behavioral output is one viable approach to improve opioid therapy. Heat shock protein 90 (Hsp90) is a molecular chaperone protein that has recently been implicated in downstream MOR signaling within the brain in mice. Here we identify a context-dependent impact on MOR signaling in which the inhibition of Hsp90 within the spinal cord promotes morphine induced anti-nociception. We show that intrathecal and not systemic administration of the Hsp90 inhibitors 17-AAG or KU-32 amplifies morphine-induced anti-nociception in both thermal and mechanical pain models. Further, we demonstrate that the inhibition of Hsp90 allows for ERK phosphorylation after opioid treatment. ERK activation was localized within the dorsal horns of the spinal cord, which are heavily populated with primary afferents responsible for nociception. The behavioral effects observed with Hsp90 inhibitors were abolished upon intrathecal U0126 (ERK inhibitor) and cycloheximide (translation inhibitor) treatment, suggesting that downstream ERK phosphorylation and rapid protein translation are responsible for the observed amplification of anti-nociception. Quantitative proteomic analysis identified upregulated RSK with spinal cord Hsp90 inhibition, which we further found was necessary for the observed enhancement of anti-nociception. Taken together, we have uncovered a novel downstream MOR ERK/RSK cascade, localized to the spinal cord and repressed by Hsp90, whose modulation may allow for enhanced efficacy and decreased side effects during opioid therapy.

2020-04-24 | PXD015060 | Pride

Aquaporin-4 mRNA binding proteins

Project description:RNA-protein pull down and differential quantitative mass spectrometry analysis of M1 mRNA binding proteins in spinal cord of WT and M23-null mice.

2021-05-27 | PXD024792 | Pride

Transcription profiling of chicken spinal cord expression

Project description:Analysis of the expression of genes in the spinal cord using the Affymetrix whole chicken genome chip, Genes expressed in the spinal cord were sorted according to identifiable protein domains using the Ensembl chicken genome assembly and cadherin domain containing genes were then knocked down by RNAi in the spinal cord to analyse their function in spinal cord development

2009-05-08 | E-TABM-701 | biostudies-arrayexpress

Time series gene expression data from adult rat tail MNs following spinal cord transection

Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearance of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomena we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immediate flaccid paralysis of the tail and a subsequent appearance of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after complete spinal transection. Tail MNs were retrogradely labelled with Fluoro-Gold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snap-frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons were laser dissected into a collector tube to a total of ca. 50-200 cells pr sample. RNA was then extracted, two round amplified and hybridized to Affymetrix rat 230 2.0 arays. 31 samples were hybridized onto chips, 4 Spi-0 (Control), 6 Spi-2, 5 Spi-7, 8 Spi-21 and 8 Spi-60.

2010-05-27 | E-GEOD-19701 | biostudies-arrayexpress

Mass spectrometry data supporting "Mass spectrometry imaging of SOD1 protein-metal complexes in SOD1G93A transgenic mice implicates demetalation with pathology"

Project description:Protein-metal complexes implicated in the pathogenesis of amyotrophic lateral sclerosis were mapped by mass spectrometry imaging. Metal-deficient hSOD1G93A complexes were revealed to be localised with disease pathology in the spinal cord and brain.

2024-07-15 | PXD053247 | Pride

Quantitative proteomic analysis of cellular nuclear protein TMT markers from rat spinal cord tissue samples in neuropathic pain model

Project description:To further reveal the mechanism of neuropathic pain, we simulated neuropathic pain by constructing a chronic constriction injury of the sciatic nerve (CCI) model, followed by quantitative proteomic analysis of rat spinal cord cell nuclei at 1 day, 7 days and sham-operated groups after CCI. A total of 3 samples from each group were used. A total of 5039 proteins were identified in this study, of which 4469 proteins contained quantitative information. Differential proteins were defined by a threshold of change >1.3-fold and t-test p-value <0.05.v

2023-01-17 | PXD034960 | Pride

Differential gene expression following SCI in trkB.T1 null

Project description:We asked what genes are significantly differentially regulated in the spinal cord of SCI trkB.T1 WT and trkB.T1 KO mice. TrkB.T1 is upregulated shortly after SCI although the precise mechanisms underyling this upregulation are poorly understood. In the trkB.T1 null, we show less mechanical allodynia and better locomotor recovery following SCI. The microarray studies helped us to elucidate a signaling pathway that is differently regulated in the WT versus KO mice at 1 day after SCI. In this study, we did not examine gene changes within a genotype after SCI. Rather, we examined DGE by genotype at each time point. Spinal cord tissue from WT and KO mice in a sham condition (intact spinal cord) versus 1D, 3D and 7D following SCI was harvested for microarray analyses.

2015-12-07 | E-GEOD-42828 | biostudies-arrayexpress

Proteomic analysis of the spatiotemporal based molecular kinetics of acute spinal cord injury identifies a time- and segment-specific window for effective tissue repair.

Project description:Spinal cord injury (SCI) represents a major debilitating health issue with a direct socioeconomic burden on the public and private sectors worldwide. Although several studies have been conducted to identify the molecular progression of injury sequel due from the lesion site, still the exact underlying mechanisms and pathways of injury development have not been fully elucidated. In this work, based on OMICs, 3D MALDI imaging, cytokines arrays, confocal imaging we established for the first time that molecular and cellular processes occurring after spinal cord injury (SCI) are altered between the lesion proximity, i.e., rostral and caudal segments nearby the lesion (R1-C1) whereas segments distant from R1-C1, i.e., R2-C2 and R3-C3 levels co-expressed factors implicated in neurogenesis. Delay in T regulators recruitment between R1 and C1 favor discrepancies between the two segments. This is also reinforced by presence of neurites outgrowth inhibitors in C1, absent in R1. Moreover, the presence of immunoglobulins (IgGs) in neurons at the lesion site at 3 days, validated by mass spectrometry, may present additional factor that contributes to limited regeneration. Treatment in vivo with anti-CD20 one hour after SCI did not improve locomotor function and IgG expression. These results open the door of a novel view of the SCI treatment by considering the C1 as the therapeutic target.

2016-06-08 | PXD003375 | Pride

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