Project description:The application of mechanical insults to the spinal cord results in profound cellular and molecular changes, including the induction of neuronal cell death and altered gene expression profiles. We demonstrated that spinal cord cells undergo cell death in response to cyclic tensile stresses, which were dose- and time- dependent. In addition, we have identified the up regulation of various genes, in particular of the MAPK pathway, which may be involved in this cellular response. We investigated the effect of cyclic tensile stresses on cultured spinal cord cells from E15 Sprague-Dawley rats, using the FX3000® Flexercell Strain Unit. We examined cell morphology and viability over a 72 hour time course. Microarray analysis of gene expression was performed using the Affymetrix GeneChip System®, where categorization of identified genes was performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) systems. time course
Project description:The application of mechanical insults to the spinal cord results in profound cellular and molecular changes, including the induction of neuronal cell death and altered gene expression profiles. We demonstrated that spinal cord cells undergo cell death in response to cyclic tensile stresses, which were dose- and time- dependent. In addition, we have identified the up regulation of various genes, in particular of the MAPK pathway, which may be involved in this cellular response. We investigated the effect of cyclic tensile stresses on cultured spinal cord cells from E15 Sprague-Dawley rats, using the FX3000® Flexercell Strain Unit. We examined cell morphology and viability over a 72 hour time course. Microarray analysis of gene expression was performed using the Affymetrix GeneChip System®, where categorization of identified genes was performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) systems.
Project description:To investigate the physiologic responses of whole osteoarthritic synovium to cycle tensile strain. We obtained 3 matched synovial tissue samples from 6 patients undergoing total knee arthroplasty, subjected them to cyclic tensile strain, and then performed gene expression profiling analysis using RNA seq from each cyclic tensile strain protocol.
Project description:Traumatic spinal cord injury (SCI) often leads to loss of locomotor function. Neuroplasticity of spinal circuitry underlies some functional recovery and therefore represents a therapeutic target to improve locomotor function following SCI. However, the cellular and molecular mechanisms mediating neuroplasticity below the lesion level are not fully understood. The present study performed a gene expression profiling in the rat lumbar spinal cord at 1 and 3 weeks after contusive SCI at T9 compared to control rat that received sham injury (laminectomy). The below-level gene expression profiles were compared with those of animals that were subjected to treadmill locomotor training. Rat lumbar spinal cords were taken for the microarray analysis at 1 and 3 weeks after contusive spinal cord injury at the T9 level. Another group of rats received treadmill locomotor training for 3 weeks, and theirs spinal cords were harvested for the microarray. The changes in gene expression after spinal cord injury were analyzed at the two time points. The influence of treadmill locomotor training was evaluated by comparing gene expression profiles between animals with or without treadmill training.
Project description:To investigate the mechanism of electrical stimulation in the repair of spinal cord injury, we established a rat model of spinal cord injury. Then, we used RNA-SEQ data obtained from ES treatment and 6 different rat models of spinal cord injury for gene expression profile analysis.
Project description:To determine whether the expression levels of circular RNAs were altered and lay a foundation for future work, we used high-throughput microarray analysis to screen circular RNAs expression patterns in the spinal cord of adult rats after traumatic spinal cord injury (SCI), finally to evaluate the potential rat models as a platform for the development of novel therapeutic targets for spinal cord injury in future clinical studies. Overall six rats at 3 days post-SCI in two groups were used to perform the microarray.
Project description:Stem cells have received substantial interest both for their potential as in vitro tools to study development and as potential therapeutic agents in a range of degenerative diseases of the nervous system. We have generated clonal neural stem cell lines from human foetal spinal cord conditionally immortalised with 4-hydroxy tamoxifen inducible cMyc (cMycERTAM), and performed a detailed assessment of their identity in terms of their expression of homeodomain transcription factors and their capacity to generate particular neuronal subtypes of the spinal cord. These lines retain a ventral spinal cord progenitor phenotype and give rise to electrically active neuronal subtypes characteristic of specific ventral progenitor subdomains. Upon grafting into lesioned rat spinal cord these cells differentiate into ChAT+ve motorneurons and show robust survival after 4 months. Total RNA was obtained from three proliferative undifferentiated neural stem cell lines at 75% confluence in culture. Two replicates of each clonal line were generated for microarray analysis.
Project description:The initiation and/or progression of ossification of the posterior longitudinal ligament (OPLL) is associated with cyclic tensile strain, but the pathomechanism of OPLL remains unclear. Indian hedgehog (Ihh) and its related signaling are key factors in normal enchondral ossification. However, the relation of OPLL to Ihh is unclear. The purpose of this study is to investigate the contribution of mechanical strain to OPLL and the relation of Ihh to OPLL. Cultured posterior longitudinal ligament cells were subjected to 24 hours of cyclic tensile strain and then analyzed by microarray.
Project description:The aneurysm clip impact-compression model of spinal cord injury (SCI) in animals mimics the primary mechanism of SCI in human, i.e. acute impact and persisting compression; and its histo-pathological and behavioural outcomes are extensively similar to the human SCI. In order to understand the distinct molecular events underlying this injury model, an analysis of global gene expression of the acute, subacute and chronic stages of a moderate to severe injury to the rat spinal cord was conducted using a microarray gene chip approach. Rat thoracic spinal cord (T7) was injured using aneurysm clip impact-compression injury model and the epicenter area of injured spinal cord was isolated for RNA extraction and processing and hybridization on Affymetrix GeneChip arrays.
Project description:In the present study, we sought to understand the impact of obesity/metabolic disease (high-fat induced) on spinal cord injury (SCI) by examining transcriptome. Adult, male Long Evans rats received either thoracic level contusion of the spinal cord or sham laminectomy and then were allowed to recover on normal rat chow for 4 weeks and further on HFD for an additional 8 weeks. Spinal cord tissues harvested from the rats were processed for Affymetrix microarray and further transcriptomic analysis.