RNA-Seq Time-Course of Rat Bladder Transcriptomes Following Spinal Cord Injury
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PROVIDER: PRJNA1252051 | ENA |
REPOSITORIES: ENA
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Project description:Spinal cord injury (SCI) evokes profound dysfunction in hollow organs such as the urinary bladder and gut. Current treatments are limited by a lack of molecular data to inform novel therapeutic avenues. Previously, we showed systemic treatment with the neuroprotective agent inosine improved bladder function following SCI in rats. This RNA-seq dataset captures global transcriptomic changes in the rat bladder at multiple time points following spinal cord injury (SCI). Full-thickness bladder tissues were collected from male Sprague Dawley rats at 2, 8, and 16 weeks post-complete T8 spinal cord transection, alongside non-injured controls.
2025-07-09 | GSE294927 | GEO
Project description:Previously, we demonstrated using a rat model of spinal cord injury (SCI) that bladder wall tissue compliance significantly increased within the first 2 weeks following injury. In order to explore the potential molecular-level mechanisms of this event, the present study quantified molecules pertinent to bladder tissue remodeling and changes in mechanical properties. An initial gene array analysis followed by real-time qPCR revealed that the message levels for tropoelastin and lysyl oxidase were as high as 8-fold in SCI rats compared to normal. Furthermore, both the message and protein levels of TGF-beta1 and IGF-1, known stimulators of elastin synthesis, in SCI rat bladders were significantly higher compared to those of normal rats. Taken together, it can be speculated that functional changes of the bladder associated with SCI induce release of select growth factors, which, in turn, stimulate elastogenesis that lead to alteration of biomechanical properties of the wall tissue.
2008-12-25 | GSE14096 | GEO
Project description:Neurogenic detrusor overactivity (NDO) is a frequent complication of spinal cord injury (SCI), often accompanied by profound structural and functional changes in the bladder. While inosine has previously been shown to improve bladder function in SCI models, its molecular effects on the bladder remain largely unexplored. In this study, we performed transcriptomic profiling of bladder tissues from SCI rats treated with inosine or vehicle. Bladder compartments were microdissected into detrusor and mucosa to capture compartment-specific changes. SCI induced widespread transcriptional alterations in both compartments, with inosine treatment partially restoring gene expression patterns toward those observed in non-injured controls. Unsupervised clustering and principal component analyses confirmed distinct transcriptional profiles associated with injury and treatment. Notably, inosine influenced a set of genes consistently altered by SCI, suggesting a protective or regulatory role at the molecular level. These findings reveal a compartment-specific transcriptomic response to spinal cord injury and provide insight into the mechanisms by which inosine may exert its therapeutic effects on the injured bladder.
2025-07-09 | GSE294930 | GEO
Project description:Purpose: The goal of this study was to determine the gene expression changes that occur over 7 days in parralyzed muscle in response to isometric contraction elicited by electrical stimulation initiated 4 months after spinal cord injury and to compare such changes to those observed in a normal muscle subjected to overload. Methods: Electrical stimulation of the soleus and plantaris muscle was stimulated in female rats with complete transection of the spinal cord at the interspace between the 9th and 10th thoracic vertebrae. Stimulation was begun 16 weeks after spinal cord transection and produced near-isometric contraction of soleus, plantaris and tibialis anterior. Muscle was analyzed at 1, 2 and 7 days after starting exercise with electrical stimulation. To provide a baseline reference for gene expression at 16 weeks after spinal cord injury, muscle was also analysed from an additional group of spinal cord transected animals. One additional group of animals with a sham-spinal cord injury was included to provide information about gene expression in neurologically intact animals of similar age. In parallel studies, rats underwent bilateral gastrocnemius ablation to overload soleus and plantaris, or a sham ablation as a control. Muscle was analyzed at 1, 3 and 7 days after gastrocnemius ablation or sham-ablation. Gene expression was determined using Affymetrix Rat Exon microarrays. For each group of animals, microarray analysis was performed for soleus muscle for each of 3 separate animals, using one array per animal. Control sammples for the spinal cord injured groups included a group of animals with a Sham-spinal cord injury, and a group of spinal cord injured animals that did not get electrical stimulation. The comparator for determining fold-change expression values was the spinal cord injured group that did not receive electrical stimulation. For each day after gastrocnemius ablation, a control was included that received all procedures needed for this ablation except cutting the distal insertion of the gastrocnemius into the Achilles tendon to control for effects of the surgery on gene expression.
2013-03-30 | E-GEOD-37476 | biostudies-arrayexpress
Project description:This study investigates the molecular changes in the bladder following spinal cord injury (SCI) in rats and the impact of inosine treatment using a multi-omics approach. We discovered the activation of PARP (Poly(ADP-ribose) polymerase) in response to SCI, a previously unrecognized phenomenon, and its attenuation with inosine treatment. SCI triggered significant DNA damage and oxidative stress pathways, whereas inosine treatment prevents DNA damage and inhibits PARP activation, offering a potential therapeutic avenue. The integrated analysis of transcriptomics and proteomics data revealed concordant regulation of multiple pathways following SCI, including EIF2 signaling and NRF2-mediated oxidative stress response, which are ameliorated by inosine treatment. These findings have relevance to human neurogenic bladder pathobiology. Pathway inhibition by inosine in the setting of SCI suggests its potential for neuroprotection in the bladder. Despite limitations, such as the focus on male rats and a lack of proteomics data from separated detrusor and mucosa, this study provides valuable insights into the molecular mechanisms underlying bladder dysfunction following SCI. It also suggests the repurposing of FDA-approved PARP inhibitors for the treatment of bladder dysfunction following spinal injury.
2025-07-14 | PXD046096 | Pride
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalizaion. To understand the moleclar mechanism behind this pheneomona we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after comlete spinal transection.
2010-05-01 | GSE19701 | 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.
2007-10-08 | E-GEOD-2270 | biostudies-arrayexpress
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:Label-free mass spectrometry-based quantitative proteomics was applied to a larval zebrafish spinal cord injury model, which allows axon regeneration and functional recovery within two days (days post lesion; dpl) after a spinal cord transection in 3 day-old larvae (dpf). Proteomic profiling was performed of the lesion site at 1 dpl in control animals and animals with pdgfrb+ cell-specific overexpression of either zebrafish chondoradherin (chad; chad-mCherry fusion), fibromodulin a (fmoda; fmoda-mCherry fusion), lumican (lum; lum-mCherry fusion) or prolargin (prelp; prelp-mCherry fusion).
2023-09-06 | PXD037605 | Pride
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearance of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomena we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immediate flaccid paralysis of the tail and a subsequent appearance of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after complete spinal transection. Tail MNs were retrogradely labelled with Fluoro-Gold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snap-frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons 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 Affymetrix rat 230 2.0 arays. 31 samples were hybridized onto chips, 4 Spi-0 (Control), 6 Spi-2, 5 Spi-7, 8 Spi-21 and 8 Spi-60.
2010-05-27 | E-GEOD-19701 | biostudies-arrayexpress