SNAP25 Ameliorates Sensory Deficit in Rats with Spinal Cord Transection

Wang, Wei; Wang, Fang; Liu, Jia; Zhao, Wei; Zhao, Qi; He, Min; Qian, Biao; Xu, Yang; Liu, Ran; Liu, Sujuan; Liu, Wei; Liu, Jin; Zhou, Xin‐Fu; Wang, Ting‐Hua

doi:10.1007/s12035-014-8642-8

Cited by 26 publications

(13 citation statements)

References 46 publications

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“…This explains for the upregulation of JUN observed in the present study, confirming the neuronal injury after SCI. SNAP25 is a component of the trans-SNARE complex, relating to membrane fusion (23), which has been reported to ameliorate the sensory deficit in rats with SCI (24). The downregulation of SNAP25 expression in the present study may therefore be associated with the sensory deficit after SCI.…”

Section: Discussionmentioning

confidence: 99%

Regulation of gene expression in rats with spinal cord injury based on microarray data

Chen

Fang

Meng

2015

Molecular Medicine Reports

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The present study aimed to investigate the molecular mechanisms of spinal cord injury (SCI) in rats. First, the differentially expressed genes (DGEs) were screened based on GSE45006 microarray data downloaded from Gene Expression Omnibus using the significant analysis of microarray (SAM) method. Screening was performed for DEGs which were negatively or possibly correlated with time and subsequently subjected to gene ontology (GO) functional annotation. Furthermore, pathway enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes was also performed. In addition, a protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins database. Finally, GeneCodis was used to seek transcription factors and microRNAs that are involved in the regulation of DEGs. A total of 806 DEGs were upregulated and 549 DEGs were downregulated in the rats with SCI. Cholesterol metabolism-associated genes (e.g. HMGCS1, FDFT1 and IDI1) were negatively correlated with time, while injury genes (e.g. SERPING1, C1S and RAB27A) were positively correlated with time after SCI. PCNA, MCM2, JUN and SNAP25 were the hub proteins of the PPI network. The transcription factors LEF1 and SP1 were observed to be associated with the regulation of two DEGs that were involved in the cholesterol-associated metabolism as well as injury responses. A number of microRNAs (e.g. miR210, miR-487b and miR-16) were observed to target cholesterol metabolism-associated DGEs. The hub genes PCNA, MCM2, JUN and SNAP25 presumably have critical roles in rats with SCI, and the transcription factors LEF1 and SP1 may be important for the regulation of cholesterol metabolism and injury responses following SCI.

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Section: Discussionmentioning

confidence: 99%

Regulation of gene expression in rats with spinal cord injury based on microarray data

Chen

Fang

Meng

2015

Molecular Medicine Reports

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“…Regardless of whether the spinal cord injury is complete or partial, aberrant sensations, including paresthesia, dysesthesia, and chronic neuropathic pain, always develop within a few months after injury [ 2 ]. Aberrant sensations are torturous experience that may make the patients suffer more serious impairments in daily life than dyskinesia alone [ 3 ]. Evidence from previous research suggests that aberrant sensations could affect cortical arousal and subsequently induce cognitive deficiency [ 4 ] and psychological problems [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury

et al. 2015

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Spinal cord injury (SCI), which is a leading cause of disability in modern society, commonly results from trauma. It has been reported that application of sciatic nerve conditioning injury plays a positive role in repairing the injury of the ascending spinal sensory pathway in laboratory animals. Because of the complexity of SCI and related ethics challenges, sciatic nerve conditioning injury cannot be applied in clinical therapy. Accordingly, it is extremely important to study its mechanism and develop replacement therapy. Based on empirical study and clinical trials, this article suggests that miR-142-3p is the key therapeutic target for repairing sensory function, based on the following evidence. Firstly, studies have reported that endogenous cAMP is the upstream regulator of 3 signal pathways that are partially involved in the mechanisms of sciatic nerve conditioning injury, promoting neurite growth. The regulated miR-142-3p can induce cAMP elevation via adenylyl cyclase 9 (AC9), which is abundant in dorsal root ganglia (DRG). Secondly, compared with gene expression regulation in the injured spinal cord, inhibition of microRNA (miRNA) in DRG is less likely to cause trauma and infection. Thirdly, evidence of miRNAs as biomarkers and therapeutic targets in many diseases has been reported. In this article we suggest, for the first time, imitating sciatic nerve conditioning injury, thereby enhancing central regeneration of primary sensory neurons via interfering with the congenerous upstream regulator AC9 of the 3 above-mentioned signal pathways. We hope to provide a new clinical treatment strategy for the recovery of sensory function in SCI patients.

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“…Within months after SCI, sensory dysfunctions, like paresthesia, dysesthesia, and chronic neuropathic pain, develops and tortures the patients day in and day out (Hao et al, ; Hongyun Huang et al, ; Hoschouer, Finseth, Flinn, Basso, & Jakeman, ; Kang et al, ; T. Wang, Yuan, Liu, Zhang, Wang, Zhou et al, ). The torture experience impairs the quality of daily life (W. Wang et al, ). Moreover, cognitive deficiency and mental impair might develop due to sensory dysfunctions (Krishnan, Glass, Turner, Watt, & Fraser, ; Richards, Hirt, & Melamed, ).…”

Section: Introductionmentioning

confidence: 99%

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Wang

et al. 2019

Journal Cellular Physiology

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Spinal cord injury (SCI) is a devastating disease. Strategies that enhance the intrinsic regenerative ability are very important for the recovery of SCI to radically prevent the occurrence of sensory disorders. Epidermal growth factor (EGF) showed a limited effect on the growth of primary sensory neuron neurites due to the degradation of phosphorylated-epidermal growth factor receptor (p-EGFR) in a manner dependent on Casitas B-lineage lymphoma (CBL) (an E3 ubiquitin-protein ligase). MiR-22-3p predicted from four databases could target CBL to inhibit the expression of CBL, increase p-EGFR levels and neurites length via STAT3/GAP43 pathway rather than Erk1/2 axis. EGF, EGFR, and miR-22-3p were downregulated sharply after injury. In vivo miR-22-3p Agomir application could regulate CBL/p-EGFR/p-STAT3/GAP43/p-GAP43 axis, and restore spinal cord sensory conductive function. This study clarified the mechanism of the limited promotion effect of EGF on adult primary sensory neuron neurite and targeting miR-22-3p could be a novel strategy to treat sensory dysfunction after SCI. K E Y W O R D Scasitas b-lineage lymphoma, epidermal growth factor, epidermal growth factor receptor, miR-22-3p, primary sensory neuron, spinal cord injury

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SNAP25 Ameliorates Sensory Deficit in Rats with Spinal Cord Transection

Cited by 26 publications

References 46 publications

Regulation of gene expression in rats with spinal cord injury based on microarray data

Regulation of gene expression in rats with spinal cord injury based on microarray data

miR-142-3p is a Potential Therapeutic Target for Sensory Function Recovery of Spinal Cord Injury

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

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