Transcription profiling of chicken spinal cord expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Gallus gallus
SUBMITTER: Dr Van Hateren
PROVIDER: E-TABM-701 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2010-10-19 | E-GEOD-20460 | biostudies-arrayexpress
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.
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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
Project description:Mice lacking the developmental axon guidance molecule EphA4 have previously been shown to exhibit extensive axonal regeneration and functional recovery following spinal cord injury. To assess mechanisms by which EphA4 may modify the response to neural injury, a microarray was performed on spinal cord tissue from mice with spinal cord injury and sham injured controls. RNA was purified from spinal cords of adult EphA4 knockout and wild-type mice four days following lumbar spinal cord hemisection or laminectomy only and was hybridised to Affymetrix All-Exon Array 1.0 GeneChips. While subsequent analyses indicated that several pathways were altered in EphA4 knockout mice, of particular interest was the attenuated or otherwise altered expression of a number of inflammatory genes, including Arginase 1, expression of which was lower in injured EphA4 knockout compared to wild-type mice. Immunohistological analyses of different cellular components of the immune response were then performed in injured EphA4 knockout and wild-type spinal cords. While numbers of infiltrating CD3+ T cells were low in the hemisection model, a robust CD11b+ macrophage / microglial response was observed post-injury. There was no difference in the overall number or spread of macrophages / activated microglia in injured EphA4 knockout compared to wild-type spinal cords at two, four or fourteen days post-injury, however a lower proportion of Arginase-1 immunoreactive macrophages / activated microglia was observed in EphA4 knockout spinal cords at four days post-injury. Subtle alterations in the neuroinflammatory response in injured EphA4 knockout spinal cords may contribute to the regeneration and recovery observed in these mice following injury. Comparison was made between gene expression in wild-type and knockout samples both before and after injury. 3 replicates per group.
2012-05-23 | E-GEOD-34430 | biostudies-arrayexpress
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.
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