Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury
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ABSTRACT:
PROVIDER: PRJNA1145954 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30174632_1.fastq.gz | Fastqsanger.gz | |||
| SRR30174632_2.fastq.gz | Fastqsanger.gz | |||
| SRR30174633_1.fastq.gz | Fastqsanger.gz | |||
| SRR30174633_2.fastq.gz | Fastqsanger.gz | |||
| SRR30174634_1.fastq.gz | Fastqsanger.gz |
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Project description:Spinal cord injury (SCI) is a debilitating condition within the nervous system with a high disability rate and substantial economic burden. The functional recovery following SCI is enhanced by moderate levels of autophagy but hindered when autophagy becomes excessive. Galectin-3 (GAL3) has been recognized as an autophagy regulator; however, its role in SCI and its associated mechanism are largely unknown. Here we report that GAL3 was increased in spinal neurons and serum in SCI rats, and knockdown or inhibition of GAL3 promoted motor function recovery. The bioinformatics analysis showed that GAL3 is closely related to programmed cell death after SCI. Indeed, the knockdown of GAL3 resulted in a decrease in autophagy markers ATG7 and LC3 II/I ratio, along with an increase in P62 expression. Furthermore, GAL3 and cell division cycle 42 (CDC42) exhibited close associations with neuronal autophagy. Injection of CDC42 inhibitor ML141 effectively reduced GAL3-mediated enhancement of neuronal autophagy. Additionally, CDC42 was increased in spinal neurons post-SCI, and administration of ML141 decreased the expression of autophagy markers and improved motor function recovery. Importantly, elevated levels of GAL3 and CDC42 were observed in the serum of SCI patients. These findings suggest a potential interplay between GAL3 and CDC42 in regulating neuronal autophagy after SCI and indicate the therapeutic potential of targeting this pathway for enhancing recovery from spinal cord injuries.
2024-09-01 | GSE274319 | GEO
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
Project description:Amyotrophic lateral sclerosis (ALS) is an incurable disease characterized by proteinaceous aggregate accumulation and neuroinflammation culminating in rapidly progressive lower and upper motor neuron death. To interrogate cell-intrinsic and inter-cell type perturbations in ALS, single-nucleus RNA sequencing was performed on the lumbar spinal cord in the murine ALS model SOD1G93A transgenic and littermate control mice at peri-symptomatic onset stage of disease, age 90 days. This work uncovered perturbed tripartite synapse functions, complement activation and metabolic stress in the affected spinal cord; processes evidenced by cell death and proteolytic stress-associated gene sets. Concomitantly, these pro-damage events in the spinal cord co-existed with dysregulated reparative mechanisms. This work provides a resource of cell-specific niches in the ALS spinal cord and asserts that interwoven dysfunctional neuronal-glial communications mediating neurodegeneration are underway prior to overt disease manifestation and are recapitulated, in part, in the human post-mortem ALS spinal cord.
2022-02-18 | GSE173524 | GEO
Project description:Here we compare the gene expression profiles of two distict, fluorescently identified neuronal populations, the motor neruons (MN) and the decending commissural interneurons (dCIN) of the neonatal rat spinal cord isolated with laser microdissection. These two populations participate in the neuronal networks in the spinal cord where they have destinct functions in shaping (dCINs) and transferring the output to the muscles (MNs) during locomotion. We wished to determine how the functinal differences in these nerurons are manifested at the gene expression level. Experiment Overall Design: Neurons were retrogradely labelled with rhodamine through application of the tracer to cut axons followed by incubation in oxygenated Ringer solution. Spinal cord were then snap frozen, cryosectioned and fluorescent single cells 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 Affymatrix RNU-34 chips. 22 samples were hybridized onto chips, 7 MNs, 7 CINS and 8 MIX.
2008-06-16 | E-GEOD-9439 | biostudies-arrayexpress
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.
2010-10-19 | GSE20460 | 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. Analysis of the areas directly (spinal cord) and indirectly (raphe and sensorimotor cortex) affected by injury will help understanding mechanisms of SCI. Hypothesis: Areas of the brain primarily affected by spinal cord injury are the Raphe and the Sensorimotor cortex thus gene expression profiling these two areas might contribute understanding the mechanisms of spinal cord injury. Specific Aim: The project aims at finding significantly altered genes in the Raphe and Sensorimotor cortex following an induced moderate spinal cord injury in T9. Keywords: other
2005-02-11 | GSE2270 | GEO
Project description:Neonatal spinal cord tissues exhibit remarkable regenerative capabilities as compared to adult spinal cord tissues after injury, but the role of extracellular matrix (ECM) in this process has remained elusive. Here, we found that early developmental spinal cord had higher levels of ECMproteins associated with neural development and axon growth, but fewer inhibitory proteoglycans, compared to those of adult spinal cord. Decellularized spinal cord ECM from neonatal (DNSCM) and adult (DASCM) rabbits preserved these differences. DNSCM promoted proliferation, migration, and neuronal differentiation of neural progenitor cells (NPCs) and facilitated axonal outgrowth and regeneration of spinal cord organoids more effectively than DASCM. Pleiotrophin (PTN) and Tenascin (TNC) inDNSCMwere identified as contributors tothese abilities. Furthermore,DNSCMdemonstrated superior performance as a delivery vehicle forNPCs and organoids in spinal cord injury (SCI)models. This suggests that ECMcues from early development stages might significantly contribute to the prominent regeneration ability in spinal cord.
2024-03-01 | GSE242908 | GEO
Project description:Despite the recognized importance of the spinal cord in sensory processing, motor behaviors, and/or neural diseases, the underlying organization of neuronal clusters remain elusive. Recently, several studies have attempted to define the neuronal types and functional heterogeneity in the spinal cord using single-cell and/or single-nucleus RNA-sequencing in various animal models. However, molecular evidence of neuronal heterogeneity in the human spinal cord has not yet been established. Here, we sought to classify spinal cord neurons from human donors using high-throughput single-nucleus RNA-sequencing. The functional heterogeneity among the identified cell types and signaling pathways that connect neuronal subtypes were explored. Moreover, we compared the transcriptional patterns obtained in human samples with previously published single-cell transcriptomic profiles of the mouse spinal cord. As a result, we generated the first comprehensive transcriptomic atlas of human spinal cord neurons and defined 18 neuronal clusters. In addition to identifying new and functionally distinct neuronal subtypes, our results also provide novel marker genes for previously described neuronal types. The comparison with mouse transcriptomic profiles revealed an overall similarity in the cellular composition of the spinal cord between the two species, while simultaneously highlighting some degree of heterogeneity. In summary, these results illustrate the complexity and diversity of neuronal types in the human spinal cord and provide an important resource for future research to explore the molecular mechanisms underlying spinal cord physiology and diseases.
2022-11-07 | GSE188255 | GEO
Project description:Neuronal–Glial Communication Perturbations in Murine SOD1G93A Spinal Cord
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Project description:Here we compare the gene expression profiles of two distict, fluorescently identified neuronal populations, the motor neruons (MN) and the decending commissural interneurons (dCIN) of the neonatal rat spinal cord isolated with laser microdissection. These two populations participate in the neuronal networks in the spinal cord where they have destinct functions in shaping (dCINs) and transferring the output to the muscles (MNs) during locomotion. We wished to determine how the functinal differences in these nerurons are manifested at the gene expression level. Keywords: Cell type comparison.
2008-03-31 | GSE9439 | GEO