Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

74 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from adult wistar female rat 5mm spinal cord tissue

ABSTRACT: We used microarray gene expression analyses to unveil the mechanisms underlying NT-3-chitosan-induced spinal cord regeneration. Complete transaction of thoracic spinal cord at T7/8 was performed, with a 5 mm segment of the spinal cord being removed. The emptied space where either refilled with a 5mm chitosan tube loaded with or without NT-3 (NT-3 or empty tube, ET, respectively) or left alone (lesion control, LC). At 1, 3, 10, 20, 30, 60, 90days post surgery, animals were sacrificed, and 5mm segments of spinal cord at the lesion site, as well as immediately caudal or rostral to the lesion segment were collected labeled with R for rostral, C for caudal, and M for lesion site

ORGANISM(S): Rattus norvegicus

SUBMITTER: Weihong Ge

PROVIDER: E-GEOD-69334 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Transcriptome analyses reveal molecular mechanisms underlying functional recovery after spinal cord injury.

Duan Hongmei H Ge Weihong W Zhang Aifeng A Xi Yue Y Chen Zhihua Z Luo Dandan D Cheng Yin Y Fan Kevin S KS Horvath Steve S Sofroniew Michael V MV Cheng Liming L Yang Zhaoyang Z Sun Yi E YE Li Xiaoguang X

Proceedings of the National Academy of Sciences of the United States of America 20151012 43

Spinal cord injury (SCI) is considered incurable because axonal regeneration in the central nervous system (CNS) is extremely challenging, due to harsh CNS injury environment and weak intrinsic regeneration capability of CNS neurons. We discovered that neurotrophin-3 (NT3)-loaded chitosan provided an excellent microenvironment to facilitate nerve growth, new neurogenesis, and functional recovery of completely transected spinal cord in rats. To acquire mechanistic insight, we conducted a series o ...[more]

PMID: 26460053

Similar Datasets

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

Patterns of gene Expression during the Spinal cord Injury/Regeneration

Project description:Spinal cord injury (SCI) induces a sequence of endogenous autodestructive changes known as secondary injury, as well as reactive biochemical changes that are neuroprotective and/or promote recovery. All these responses to SCI are, in part re?ected in changes in gene expression. In order to assess changes in gene expression involved in the regeneration process,microarrays were performed as a function of time after SCI for the various treatments. Three groups rats(i.e.NT-3-chitosan tube group, tube alone group and lesion control group) used to interrogate Affymetrix (SantaClara,CA) GeneChips were sacrificed by intraperitoneally over dose injecting 6% chloral hydrate at 1, 3, 10, 20, 30, and 90 d after the operation. The spinal cords were surgically re-exposed and spinal tissue including dura and meninges was dissected into three blocks, i.e. 5 mm long segments in the lesioned area (M), rostral to the lesioned area (R), and caudal to the lesioned areas (C) were sampled under RNAase-free conditions. The samples were quick frozen and kept in liquid nitrogen.

2012-01-01 | E-GEOD-29488 | biostudies-arrayexpress

Transcription profiling of mouse E12.5 ePet-EYFP rostral and caudal serotonin (5HT) neurons purified by flow cytometry

Project description:The 5HT system is organized into rostral and caudal populations with discrete anatomical locations and opposite axonal trajectories in the developing hindbrain. 5HT neuron cell bodies in the rostral subdivision migrate to the midbrain and pons and extend ascending projections throughout the forebrain. 5HT cell bodies in the caudal subdivision migrate to the ventral medulla and caudal half of the pons and provide descending projections to the brainstem and spinal cord. Experiment Overall Design: We used microarrays to determine genes expressed by both rostral and caudal 5HT neurons as well as genes that are differentially expressed between rostral and caudal 5HT neurons at E12.5 when axon pathfinding and cell migration are underway. E12.5 neural tubes were isolated from ePet-EYFP embryos and dissected into a rostral domain (mesecephalic flexure to pontine flexure) and a caudal domain (pontine flexure to spinal cord). After cell dissociation (details under growth protocol), cells were subjected to fluorescent activated cell sorting (FACS) to obtain 4 cell populations. R+ = rostral ePetEYFP positive 5HT neurons; R- = YFP negative non-serotonergic cells in the rostral neural tube; C+ = caudal ePetEYFP positive 5HT neurons; C- = YFP negative non-serotonergic cells in the caudal neural tube. 200,000 cells for each of the 4 cell types (R+, R-, C+, C-) were collected for RNA extraction and hybridization to Affymetrix Mouse 430 2.0 arrays.

2010-01-30 | E-GEOD-19474 | biostudies-arrayexpress

Age-dependent gene and protein expression following transection of neonatal spinal cord of Monodelphis domestica (South American Grey Short-tailed opossum)

Project description:In the present study we investigated the genome and the proteome in the segment of cord rostral to the site of injury following a complete spinal cord transection in opossums at an age when axonal growth across a lesion and substantially normal locomotor development occur (postnatal day 7, P7) and compared this with an older age when no axon growth can be seen, but nevertheless a demonstrable body weight-bearing locomotion is present (P28, Wheaton et al, 2011). 7 RNA-seq samples, consisting of 2 biological replicates of controls at day 8, 1 control sample at day 29, and 2 biological replicates each from injured animals at days 8 and 29.

2015-02-10 | E-GEOD-54805 | 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 - IgG identification

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 matrix-assisted laser desorption ionization (MALDI) imaging, cytokines arrays, confocal imaging we established for the first time that molecular and cellular processes occurring after 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 decrease 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 | PXD004247 | Pride

Expression data from adult wistar female rat 5mm spinal cord tissue

Project description:We used microarray gene expression analyses to unveil the mechanisms underlying NT-3-chitosan-induced spinal cord regeneration.

2015-11-02 | GSE69334 | GEO

RhoA inhibitor treatment of spinal cord injury: Deep inside mechanism understanding for a better use

Project description:The present study shows by in vivo experiments, the impact of RhoA inhibitor treatment using a functionalized alginate scaffold and the beneficial results at the early stage by increasing neurites outgrowth and synaptic contact. However, 7 days after treatment a plateau is obtained in BBB score. We thus performed an in vitro and proteomic associated to systemic biology analyses of secreted factors from ND7/23 DRG cell line incubated with secreted factors from different segments after spinal cord lesion treated wih RhoA inhibitor. We then performed a time course proteomic study from the DRG cells in same conditions as for the secretome. The results taken together allow a better understanding of the mechanisms occurring in both side of the lesion and led a positive impact of the treatment on growth cone guidance in both sides of the lesion (Rostral 1 and Caudal 1). We identified the transcription factors involved in time course at the beginning of the treatment and the growth cone factors (receptors, ligands, signaling pathways) implicated in this time course. We also demonstrate the involvement of immunoglobulins (IgG1, IgG2) in this process. Anti-GFAP seem to bind to its own receptor in DRG cells when neurite outgrowth is initiated and thus modulate the process like in traumatic brain injury. These results open the door of a concomitant treatment at both sides of the lesion with RhoA inhibitor. However, we also pointed that RhoA inhibitor treatment led to an inhibition of several factors implicated in neurogenesis reflecting a global inhibition at term as detected in vivo that reached 2 weeks after treatment. RhoA inhibitor treatment is useful to initiate the neurogenesis process but needs to be supplied by a second treatment for increasing synaptic connections and the neuron reconnections.

2017-07-28 | PXD004639 | Pride

Expression data from E12.5 ePet-EYFP rostral and caudal serotonin (5HT) neurons purified by flow cytometry

2009-12-16 | GSE19474 | GEO

Next Generation Sequencing of zebrafish V2a interneurons in spinal segments rostral to the lesion after spinal cord injury

Project description:The goals of this study is to compare transcriptome profiles (RNA-seq) of zebrafish V2a interneurons with regrown axon and those without regrown axon in the spinal segments rostral to the lesion after spinal cord injury. For purification of V2a interneurons with regrown axon, the fluorescent tracer Rhodamine Dextran (RD) was retrogradely applied to Tg(Chx10:GFP) fish at three or eight weeks post injury. Spinal cord segments rostral to the lesion site was collected from 20 fish at 3- or 8 wpi, and corresponding spinal cord segments from 20 uninjured fish were collected as control material. GFP+/RD+ and GFP+/RD- cells were FAC-sorted and subjected to RNA-sequencing. Total RNA was isolated using SMART-SeqTM v4 UltraTM Low Input RNA Kit for Sequencing (Clontech). Sequencing libraries (N=5-6) were generated using NEBNext UltraTM RNA Library Prep Kit for Illumina following the manufacturer’s instructions (NEB). We mapped about 40-80 million sequence reads per sample to the zebrafish genome and identified 42,370 transcripts in the zebrafish V2a interneurons in the spinal cord. Our study represents the detailed analysis of transcriptomes of zebrafish V2a interneurons with regrown axon and those without regrown axon in the spinal segments rostral to the lesion after spinal cord injury.

2022-09-13 | GSE213081 | GEO

Motor cortex after C3 lesion

Project description:Gene expression analysis of motor cortex after spinal C3 lesion Dorsal column wire knife lesions: Adult female Fischer 344 rats weighing 150-200 gm were used. Animals underwent a laminectomy at spinal level C3. Dorsal funiculus lesions were made in the middle of C3 using a Kopf microwire device (Kopf Instruments, Tujunga, CA). After fixation in a spinal stereotaxic unit, a small dural incision was made. The wire knife was lowered into the spinal cord to a depth of 1.1 mm ventral to the dorsal cord surface and 1.1 mm to the left of the midline. The tip of the wireknife was extruded, forming a 2.25 mm-wide arc that was raised to the dorsal surface of the cord. To ensure complete axotomy of the dorsal funiculus, spinal tissue was compressed against the microwire knife surface using a microaspiration pipette until all visible white matter was transected. Cortical microdissection: The forelimb and hindlimb motor cortex were microdisected from rat cortices: Rostral to Bregma: an area from 2.0 to 4.5 mm mediolateral and from 0 to 2 mm anterior-posterior Caudal to Bregma: an area from 2.0 to 3.5 mediolateral and from 0 to 3 mm caudal to Bregma. Only the inferior half of the cortex containing layer V corticospinal motor neurons was sampled in each region.

2016-07-01 | E-GEOD-76679 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data