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Identifiation of lncRNA expression profiles and ceRNA analysis in the spinal cord of morphine tolerance rats

ABSTRACT: Identifiation of lncRNA expression profiles and ceRNA analysis in the spinal cord of morphine tolerance rats

PROVIDER: PRJNA432908 | ENA |

REPOSITORIES: ENA

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Identifiation of lncRNA expression profiles and ceRNA analysis in the spinal cord of morphine tolerance rats

Project description:The mechanism of morphine tolerance remains unclear, and lncRNA have been promising molecule in many pathophysiological processes. However, the role of lncRNA on morphine tolerance hasn’t been explored yet. So we explore this issue, and our results indicated that the expression profiles of lncRNAs have changed in morphine tolerance rats as compared with normal rats, and among those, some differentially expressed lncRNAs might be new therapeutic targets for morphine tolerance.

2018-04-05 | GSE110115 | GEO

Circular RNA expression profile in the spinal cord of morphine tolerated rats and screen of putative key circRNAs

Project description:Microarray analysis for circRNA expression in the spinal cord was conducted and compared between 4 morphine tolerated rats and 4 normal rats

2019-07-02 | GSE133602 | GEO

Inhibition of spinal cord Hsp90 enhances morphine anti-nociception by activating an ERK/RSK pathway

Project description:Morphine and other opioids continue to be commonly utilized as clinical analgesics, despite their numerous adverse side effects, including respiratory depression, addiction, and tolerance. The modulation of µ-opioid receptor (MOR) signaling and subsequent behavioral output is one viable approach to improve opioid therapy. Heat shock protein 90 (Hsp90) is a molecular chaperone protein that has recently been implicated in downstream MOR signaling within the brain in mice. Here we identify a context-dependent impact on MOR signaling in which the inhibition of Hsp90 within the spinal cord promotes morphine induced anti-nociception. We show that intrathecal and not systemic administration of the Hsp90 inhibitors 17-AAG or KU-32 amplifies morphine-induced anti-nociception in both thermal and mechanical pain models. Further, we demonstrate that the inhibition of Hsp90 allows for ERK phosphorylation after opioid treatment. ERK activation was localized within the dorsal horns of the spinal cord, which are heavily populated with primary afferents responsible for nociception. The behavioral effects observed with Hsp90 inhibitors were abolished upon intrathecal U0126 (ERK inhibitor) and cycloheximide (translation inhibitor) treatment, suggesting that downstream ERK phosphorylation and rapid protein translation are responsible for the observed amplification of anti-nociception. Quantitative proteomic analysis identified upregulated RSK with spinal cord Hsp90 inhibition, which we further found was necessary for the observed enhancement of anti-nociception. Taken together, we have uncovered a novel downstream MOR ERK/RSK cascade, localized to the spinal cord and repressed by Hsp90, whose modulation may allow for enhanced efficacy and decreased side effects during opioid therapy.

2020-04-24 | PXD015060 | Pride

Epitranscriptomic map of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats

Project description:Morphine tolerance is a tricky problem, the mechanism of it is still unclear. Circular RNAs (CircRNAs) play important roles in biological process of central nervous system. N6-methyladenosine (m6A) as a key post-transcriptional modification of RNA can regulate the metabolism and functions of circRNAs. Here we conducted this research to explore the patterns of m6A-methylation of circRNAs in the spinal cords of 4 morphine tolerated rats and 4 normal rats.

2022-04-05 | GSE199892 | GEO

Epitranscriptomic map of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats

Project description:Epitranscriptomic map of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats

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Chronic contusion spinal cord injury in rats

Project description:Excerpt from a larger study which characterized the transcriptional effects of a spinal cord contusion injury in rats. This is the data from the almost chronic contusion state (35 days) at the injury site (Thoracic 8) - where we saw significant changes in several areas, including cholesterol metabolism genes. Other spinal cord areas (rostral, caudal) and time-points (3 hours, 24 hours, 7 days and 35 days) were analyzed as well and are discussed in our paper and at www.crpf.org/microarray. Keywords = Spinal Cord Injury Keywords = chronic Keywords = thoracic Keywords = cholesterol Keywords: repeat sample

2005-05-03 | GSE2599 | GEO

Spinal cord injury

Project description:Spinal cord injury

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EZH2 drives transcriptional repression of trpc5 gene in morphine tolerance

Project description:Purpose: To identify differentially expressed genes regulated by morphine in mice. Methods: Mice were intrathecally injected with normal saline or morphine (10 ug/10 uL) for 7 days and then spinal cords L4-L5 were collected and subjected to mRNA-sequencing by geneseeq and data analysis. Results: We identified morphine upregulated 42 genes and downregulated 44 genes compared with saline group. KEGG enrichment analysis showed calcium signaling pathway was downregulated by morphine and we noticed that TRPC5 was one of the most significantly downregulated genes by morphine. We confirmed that intrathecal injection of morphine leads to Trpc5 transcriptional suppression via reducing GABA release, contributing to morphine tolerance.

2024-12-31 | GSE246582 | GEO

An aptamer-based bionic spinal cord scaffold elicits robust neurogenesis in situ after spinal cord injury in rats

Project description:Transected spinal cord injury (SCI) results in significant structural disruption of the spinal cord. The reconstruction of neural pathways following SCI faces several key challenges, including inadequate endogenous neural stem cells (NSCs) and poor neurogenesis in natural repair process, and concerns related to the long-term survival of neurons following exogenous transplantation. In the current study, we report an oligonucleotide aptamer drug (Apt19S) which is first proven to recruit endogenous NSCs to the site of injury following SCI, and therefore develop a bionic spinal cord scaffold that can sustainedly release Apt19S and neurotrophin-3 (NT-3) to provide the neurogenic niche with the necessary mechanical properties and support for in situ spinal cord repair. The bionic scaffold successfully recruited a significant number of endogenous NSCs in vivo and established a neurogenic niche that was abundant in NT-3, thereby promoting neuronal differentiation and the formation of neuronal networks Regenerated nerve fibers including 5-hydroxytryptamine-positive nerve fibers and corticospinal tract grew robustly into the injury site and generated synaptic connections with the newborn neurons. Collectively, our findings indicate that our aptamer-based bionic spinal cord scaffold elicits a robust neurogenesis process in situ, breaking the limitations imposed by poor self-repair ability in the adult spinal cord.

2023-10-19 | GSE245409 | GEO

Transcriptomic analysis of ipsilateral spinal cord in rats after bone fracture

Project description:To investigate the specific changes in the spinal cord after bone fractures, we obtained L4-L5 spinal cord segments from the same side of SD rats with tibial fractures

2025-09-10 | GSE230779 | GEO

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