scholarly journals Identifying the Biomarkers of Spinal Cord Injury and the effects of Neurotrophin-3 Based on MicroRNA and mRNA Signature

2020 ◽  
Author(s):  
Shuang Qi ◽  
Zinan Li ◽  
Shanshan Yu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Molecular Mechanisms ◽  
Ion Homeostasis ◽  
Metabolic Process ◽  
Neurological Injury ◽  
Receptor Interaction ◽  
Transcription Profile ◽  
Neurotrophin 3 ◽  
Cord Injury

Abstract Background To gain a better understanding of the molecular mechanisms of spinal cord injury and the effects of Neurotrophin-3, differentially expressed microRNAs (DEmiRNAs) and genes (DEGs) were analyzed. Methods The miRNA transcription profile of GSE82195 and the mRNA transcription profile of GSE82196 were downloaded from the Gene Expression Omnibus (GEO). Then, DERs were identified using limma. The noise-robust soft clustering of the intersection DERs was performed using Mfuzz package. Additionally, the integrated miRNAs–targets regulatory network was constructed using Cytoscape. Finally, the Comparative Toxicogenomics Database 2019 update was used to search the central nervous system injury related pathway. Results A total of 444 DERs including 382 DEGs and 62 DEmiRNAs were screened between group injury and group none whlie 576 DERs including 523 DEGs and 55 DEmiRNAs were screened between group NT-3 and group injury. Moreover, 80 intersections DERs were identified. DREs in cluster 1 were firstly significantly down-regulated in group injury and subsequently were significantly up-regulated in group NT-3. DERs in cluster 2 were firstly up-regulated in group injury and subsequently down-regulated in group NT-3. OPRL1 and GHSR were enriched in the KEGG pathway of Neuroactive ligand-receptor interaction. OPRL1 was involved in the chemical homeostasis and ion homeostasis while GHSR was related to the regulation of fatty acid metabolic process and regulation of cellular ketone metabolic process. Conclusion rno-miR-3072 and rno-miR-667-5p and OPRL1 and GHSR might participate in the pathogenesis of neurological injury and the neurotrophin-3 treatment.

scholarly journals Identifying the Biomarkers of Spinal Cord Injury and the effects of Neurotrophin-3 Based on MicroRNA and mRNA Signature

2019 ◽  
Author(s):  
Shuang Qi ◽  
Zinan Li ◽  
Shanshan Yu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Regulatory Network ◽  
Metabolic Process ◽  
Differentially Expressed ◽  
Transcription Profile ◽  
Comparative Toxicogenomics Database ◽  
Neurotrophin 3 ◽  
Cord Injury ◽  
Cluster 2

Abstract Background: To gain a better understanding of the molecular mechanisms of spinal cord injury and the effects of Neurotrophin-3, differentially expressed microRNAs (DEmiRNAs) and genes (DEGs) were analyzed. Methods: The miRNA transcription profile of GSE82195 and the mRNA transcription profile of GSE82196 including dorsal root ganglion (DRG) tissue samples of normal adult rat (none, n=6), 10 weeks post-pyramidotomy, intramuscular AAV-1 GFP (injury, n=6) and 10 weeks post-pyramidotomy, intramuscular AAV-1 prepro-neurotrophin-3 (NT-3, n=6) were downloaded from the Gene Expression Omnibus (GEO; http://www.ncbi.nlm.nih.gov/geo/). Then, differentially expressed RNAs (DERs) including DEmiRNAs and DEGs were identified using limma. The noise-robust soft clustering of the intersection DERs was performed using Mfuzz package. Additionally, the integrated miRNAs–targets regulatory network was constructed using Cytoscape. Finally, the Comparative Toxicogenomics Database 2019 update (http://ctd.mdibl.org/) were used to search the central nervous system injury related pathway. Results: A total of 444 DERs including 382 DEGs and 62 DEmiRNAs were screened between group injury and group none whlie 576 DERs including 523 DEGs and 55 DEmiRNAs were screened between group NT-3 and group injury. Moreover, 80 intersections DERs were identified.Two clusters were obtained including cluster 1 (including rno-miR-3072, rno-miR-667-5p and so on) and cluster 2 (OPRL1, GHSR and so on). DREs in cluster 1 were firstly significantly downregulated in group injury and subsequently were significantly upregulated in group NT-3. DERs in cluster 2 were firstly upregulated in group injury and subsequently downregulated in group NT-3. OPRL1 and GHSR were enriched in the KEGG pathway of Neuroactive ligand-receptor interaction which is also found in the Comparative Toxicogenomics Database 2019 update. OPRL1 was involved in the chemical homeostasis and ion homeostasis while GHSR was related to the regulation of fatty acid metabolic process and regulation of cellular ketone metabolic process. Conclusion: DEmiRNAs rno-miR-3072 and rno-miR-667-5p and DEGs OPRL1 and GHSR might participate in the pathogenesis of neurological injury and the neurotrophin-3 treatment. Keywords: spinal cord injury, differentially expressed miRNA, differentially expressed gene, regulatory network, Neurotrophin-3

scholarly journals Transcriptome analyses reveal molecular mechanisms underlying functional recovery after spinal cord injury

2015 ◽  
Vol 112 (43) ◽  
pp. 13360-13365 ◽  
Author(s):  
Hongmei Duan ◽  
Weihong Ge ◽  
Aifeng Zhang ◽  
Yue Xi ◽  
Zhihua Chen ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Cns Injury ◽  
Neurotrophin 3 ◽  
Cord Injury ◽  
Transcriptome Analyses ◽  
Regeneration Capability

Spinal cord injury (SCI) is considered incurable because axonal regeneration in the central nervous system (CNS) is extremely challenging, due to harsh CNS injury environment and weak intrinsic regeneration capability of CNS neurons. We discovered that neurotrophin-3 (NT3)-loaded chitosan provided an excellent microenvironment to facilitate nerve growth, new neurogenesis, and functional recovery of completely transected spinal cord in rats. To acquire mechanistic insight, we conducted a series of comprehensive transcriptome analyses of spinal cord segments at the lesion site, as well as regions immediately rostral and caudal to the lesion, over a period of 90 days after SCI. Using weighted gene coexpression network analysis (WGCNA), we established gene modules/programs corresponding to various pathological events at different times after SCI. These objective measures of gene module expression also revealed that enhanced new neurogenesis and angiogenesis, and reduced inflammatory responses were keys to conferring the effect of NT3-chitosan on regeneration.

Activation of SIRT1 by Hyperbaric  Oxygenation Promotes Recovery of Motor Dysfunction in Spinal Cord Injury Rats

2020 ◽  
Author(s):  
Huiqiang Chen ◽  
Mengyu Yao ◽  
Zhibo Li ◽  
Ranran Xing ◽  
Cheng Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Molecular Mechanisms ◽  
Hyperbaric Oxygenation ◽  
Rating Scale ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Inflammatory Cascade ◽  
Locomotor Function ◽  
Cord Injury

Abstract Background: Emerging evidence demonstrated that hyperbaric oxygenation (HBO) therapy improved the locomotor dysfunction following spinal cord injury (SCI). Sirtuin1(SIRT1) has been characterized as neuroprotection in nerve system. However, whether SIRT1 is involved in alleviation of locomotor function by HBO therapy is unclear. Methods: The Basso, Beattie Bresnahan (BBB) locomotor rating scale was used to evaluate the open-field locomotor function. Western blot, real-time quantitative reverse transcription polymerase chain reaction, SIRT1 activity assay and enzyme-linked immunosorbent assays were performed to explore the molecular mechanisms in adult Sprague-Dawley rats. Results: We found that series HBO therapy significantly improved the locomotor dysfunction and ameliorated the decrease mRNA, protein and activity of spinal cord SIRT1 induced by traumatic SCI injury in rats. In addition, intraperitoneal injection SIRT1 antagonist EX-527 abolished the beneficial effects of series HBO treatment on locomotor deficits and SIRT1 activity loss caused by traumatic SCI injury. However, the rats undergone both series HBO therapy and SIRT1 agonist SRT1720 got the higher BBB score than that undergone series HBO treatment only. Importantly, series HBO treatment following the traumatic SCI injury inhibited the inflammatory cascade and apoptosis-related protein, which was retained by EX-527 and enhanced by SRT1720. Furthermore, EX-527 blocked the enhanced induction of autophagy series with HBO application. Conclusion: These findings demonstrated a new mechanism for series HBO therapy involving activation of SIRT1 and subsequent modulation of inflammatory cascade, apoptosis and autophagy, which contributed to the recovery of motor dysfunction. Key words: HBO, SIRT1, motor dysfunction, inflammation, autophagy, apoptosis

scholarly journals Descending motor circuitry required for NT-3 mediated locomotor recovery after spinal cord injury in mice

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qi Han ◽  
Josue D. Ordaz ◽  
Nai-Kui Liu ◽  
Zoe Richardson ◽  
Wei Wu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Neurons ◽  
Enhanced Recovery ◽  
Neural Pathways ◽  
Locomotor Recovery ◽  
Neurotrophin 3 ◽  
Cord Injury ◽  
Dendritic Atrophy ◽  
Descending Projections

AbstractLocomotor function, mediated by lumbar neural circuitry, is modulated by descending spinal pathways. Spinal cord injury (SCI) interrupts descending projections and denervates lumbar motor neurons (MNs). We previously reported that retrogradely transported neurotrophin-3 (NT-3) to lumbar MNs attenuated SCI-induced lumbar MN dendritic atrophy and enabled functional recovery after a rostral thoracic contusion. Here we functionally dissected the role of descending neural pathways in response to NT-3-mediated recovery after a T9 contusive SCI in mice. We find that residual projections to lumbar MNs are required to produce leg movements after SCI. Next, we show that the spared descending propriospinal pathway, rather than other pathways (including the corticospinal, rubrospinal, serotonergic, and dopaminergic pathways), accounts for NT-3-enhanced recovery. Lastly, we show that NT-3 induced propriospino-MN circuit reorganization after the T9 contusion via promotion of dendritic regrowth rather than prevention of dendritic atrophy.

scholarly journals Robotic-Assisted, Body-Weight–Supported Treadmill Training in Individuals Following Motor Incomplete Spinal Cord Injury

2005 ◽  
Vol 85 (1) ◽  
pp. 52-66 ◽  
Author(s):  
T George Hornby ◽  
David H Zemon ◽  
Donielle Campbell
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Body Weight ◽  
Physical Therapists ◽  
Treadmill Training ◽  
Neurological Injury ◽  
Walking Ability ◽  
Incomplete Spinal Cord Injury ◽  
Robotic Assisted ◽  
Cord Injury

AbstractBackground and Purpose. Performance of therapist-assisted, body-weight–supported treadmill training (BWSTT) to enhance walking ability of people with neurological injury is an area of intense research. Its application in the clinical setting, however, is limited by the personnel and labor requirements placed on physical therapists. Recent development of motorized (“robotic”) rehabilitative devices that provide assistance during stepping may improve delivery of BWSTT. Case Description. This case report describes the use of a robotic device to enhance motor recovery and ambulation in 3 people following motor incomplete spinal cord injury. Interventions. Changes in motor impairment, functional limitations, and locomotor disability were monitored weekly during robotic-assisted BWSTT and following transition to therapist-assisted BWSTT with the assistance of one therapist. Outcomes. Following this training, 2 patients recovered independent over-ground walking and another improved his gait speed and endurance. Discussion. The use of robotic devices may assist physical therapists by providing task-specific practice of stepping in people following neurological injury.

scholarly journals Molecular mechanisms underlying functional recovery after spinal cord injury

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S532-S533
Author(s):  
Nadezda Lukacova ◽  
Katarina Bimbova ◽  
Andrea Stropkovska ◽  
Alexandra Kisucka ◽  
Maria Bacova ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Molecular Mechanisms ◽  
Cord Injury

Pediatric spinal injury: the very young

1988 ◽  
Vol 68 (1) ◽  
pp. 25-30 ◽  
Author(s):  
John R. Ruge ◽  
Grant P. Sinson ◽  
David G. McLone ◽  
Leonard J. Cerullo
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Spinal Injury ◽  
Causative Factor ◽  
Important Variable ◽  
Neurological Injury ◽  
Content Type ◽  
Significant Difference ◽  
Cord Injury

✓ Maturity of the spine and spine-supporting structures is an important variable distinguishing spinal cord injuries in children from those in adults. Cinical data are presented from 71 children aged 12 years or younger who constituted 2.7% of 2598 spinal cord-injured patients admitted to the authors' institutions from June, 1972, to June, 1986. The 47 children with traumatic spinal cord injury averaged 6.9 years of age and included 20 girls (43%). The etiology of the pediatric injuries differed from that of adult injuries in that falls were the most common causative factor (38%) followed by automobile-related injuries (20%). Ten children (21.3%) had spinal cord injury without radiographic abnormality (SCIWORA), whereas 27 (57%) had evidence of neurological injury. Complete neurological injury was seen in 19% of all traumatic pediatric spinal cord injuries and in 40% of those with SCIWORA. The most frequent level of spinal injury was C-2 (27%, 15 cases) followed by T-10 (13%, seven cases). Upon statistical examination of the data, a subpopulation of children aged 3 years or younger emerged. These very young children had a significant difference in level of injury, requirement for surgical stability, and sex distribution compared to 4- to 12-year-old children.

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