Effect of inhibition of oxidative stress on transcriptome profiles in rats with spinal cord injury.
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE242507 | GEO | 2024/04/29
REPOSITORIES: GEO
Similar Datasets
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 reflected 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.
2012-01-01 | GSE29488 | GEO
Project description:Hematopoietic differentiation from human pluripotent stem cell in vitro is an important approach for the research of hematopoietic stem cell regeneration. Small molecules that can maintenance low ROS level and inhibit cell apoptosis or autophagy are benifit for the maintenance or expansion of hematopoietic stem cells. Lipoic acid (ALA) as a small antioxidant molecule can regulate the ROS level and apoptosis of cells. This study found that lipoic acid promoted the production of hemogenic endothelial cells and hematopoietic progenitor cells. Transcriptome analysis of hemogenic endothelial cells showed that ALA upregulated the endothelial to hematopoietic transition (EHT) related genes and downregulated the EHT negative regulated genes. ALA also up-regulated ROS and apoptosis related genes to inhibit the apoptosis of hematopoietic stem/progenitor cells.These results indicated that ALA might have an important role in the regeneration of hematopoietic stem progenitor cell in vitro.
2020-07-14 | GSE144307 | GEO
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
Project description:Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecule inhibitors would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of alpha lipoic acid (ALA), a naturally existing antioxidant, in targeting senescent cells via induction of programmed cell death. This study demonstrates the impact of alpha-lipoic acid as a medicinal compound on the expression profile of senescent cells and provides a strong rationale for its future use in geriatric medicine.
2022-12-31 | GSE156184 | GEO
Project description:Summary: Spinal cord injury (SCI) is a damage to the spinal cord induced by trauma or disease resulting in a loss of mobility or feeling. SCI is characterized by a primary mechanical injury followed by a secondary injury in which several molecular events are altered in the spinal cord often resulting in loss of neuronal function. Hypothesis: Spinal cord injury (SCI) induces a cascade of molecular events including the activation of genes associated with transcription factors, inflammation, oxidative stress, ionic imbalance, apoptosis and neuroregeneration which suggests the existance of endogenous reparative attempts. However, not all mechanisms following SCI are well known. Specific Aim: The goal of this project is to analyze the molecular events following spinal cord injury 1 cm above, below, and at the site of injury (T9), aiming at finding potential new targets to improve recovery and therapy.
2007-09-04 | E-GEOD-464 | biostudies-arrayexpress
Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue. 2x2 model with 4 groups and 12 total samples. 2 rat strains (athymic nude [AN] and Sprague-Dawley [SD]) and 2 time points (1 week post-injury [acute] and 8 weeks post-injury [chronic]). 3 samples per group, for a total of 12 samples. No technical replicates were performed. Acute SD group = rats 618, 619, and 620. Chronic SD group = rats 605, 606, and 608. Acute AN group = rats 714, 715, and 717. Chronic AN group = rats 707, 712, and 713.
2015-10-26 | E-GEOD-62760 | biostudies-arrayexpress
Project description:Traumatic spinal cord injury (SCI) triggers a neuro-inflammatory response dominated by tissue-resident microglia and monocyte derived macrophages (MDMs). Since activated microglia and MDMs are morphologically identical and express similar phenotypic markers in vivo, identifying injury responses specifically coordinated by microglia has historically been challenging. Here, we pharmacologically depleted microglia and use anatomical, histopathological, tract tracing, bulk and single cell RNA sequencing to reveal the cellular and molecular responses to SCI controlled by microglia. We show that microglia are vital for SCI recovery and coordinate injury responses in CNS-resident glia and infiltrating leukocytes. Depleting microglia exacerbates tissue damage and worsens functional recovery. Conversely, restoring select microglia-dependent signaling axes, identified through sequencing data, in microglia depleted mice prevents secondary damage and promotes recovery. Additional bioinformatics analyses reveal that optimal repair after SCI and likely other forms of neurological disease, might be achieved by co-opting key ligand-receptor interactions between microglia, astrocytes and MDMs.
2022-06-01 | GSE196928 | GEO
Project description:This study examines the molecular effects of surgical scar resection in complete chronic spinal cord injury (SCI) through RNA sequencing. Results show that scar resection alters gene expression, with downregulation of axonal growth inhibitors and upregulation of neuroprotective genes. Additionally, the application of a decellularized extracellular matrix (dECM) hydrogel as a scaffold promoted angiogenesis. Gene Ontology analysis indicated enrichment of immune-related processes, suggesting that scar resection improves the spinal cord microenvironment for neural repair. These findings indicate the potential of combining scar resection with scaffolding to support recovery after chronic complete SCI.
2024-10-08 | GSE278491 | GEO
Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue.
2015-10-26 | GSE62760 | GEO
Project description:Summary: Spinal cord injury (SCI) is a damage to the spinal cord induced by trauma or desease resulting in a loss of mobility or feeling. SCI is characterized by a primary mechanical injury followed by a secondary injury in which several molecular events are altered in the spinal cord often resulting in loss of neuronal function. Hypothesis: Spinal cord injury (SCI) induces a cascade of molecular events including the activation of genes associated with transcription factors, inflammation, oxidative stress, ionic imbalance, apoptosis and neuroregeneration which suggests the existance of endogenous reparative attempts. However, not all mechanisms following SCI are well known. Specific Aim: The goal of this project is to analyze the molecular events following spinal cord injury 1 cm above, below, and at the site of injury (T9), aiming at finding potential new targets to improve recovery and therapy. Keywords: other
2003-07-16 | GSE464 | GEO