Ly6C+Ly6G−Myeloid-derived suppressor cells play a critical role in the resolution of acute inflammation and the subsequent tissue repair process after spinal cord injury

2013 ◽  
Vol 125 (1) ◽  
pp. 74-88 ◽  
Author(s):  
Hirokazu Saiwai ◽  
Hiromi Kumamaru ◽  
Yasuyuki Ohkawa ◽  
Kensuke Kubota ◽  
Kazu Kobayakawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Tissue Repair ◽  
Acute Inflammation ◽  
Critical Role ◽  
Suppressor Cells ◽  
Repair Process ◽  
Myeloid Derived Suppressor Cells ◽  
Cord Injury

scholarly journals Critical role of mitochondrial aldehyde dehydrogenase 2 in acrolein sequestering in rat spinal cord injury

2022 ◽  
Vol 17 (7) ◽  
pp. 1505
Author(s):  
Riyi Shi ◽  
SethA Herr ◽  
Liangqin Shi ◽  
Thomas Gianaris ◽  
Yucheng Jiao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Aldehyde Dehydrogenase ◽  
Critical Role ◽  
Aldehyde Dehydrogenase 2 ◽  
Rat Spinal Cord ◽  
Cord Injury

scholarly journals Cytokine and Growth Factor Activation In Vivo and In Vitro after Spinal Cord Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
Elisa Garcia ◽  
Jorge Aguilar-Cevallos ◽  
Raul Silva-Garcia ◽  
Antonio Ibarra
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Critical Role ◽  
Glutamate Excitotoxicity ◽  
Signaling Proteins ◽  
Neurodegenerative Process ◽  
Cord Injury ◽  
Ion Imbalance

Spinal cord injury results in a life-disrupting series of deleterious interconnected mechanisms encompassed by the primary and secondary injury. These events are mediated by the upregulation of genes with roles in inflammation, transcription, and signaling proteins. In particular, cytokines and growth factors are signaling proteins that have important roles in the pathophysiology of SCI. The balance between the proinflammatory and anti-inflammatory effects of these molecules plays a critical role in the progression and outcome of the lesion. The excessive inflammatory Th1 and Th17 phenotypes observed after SCI tilt the scale towards a proinflammatory environment, which exacerbates the deleterious mechanisms present after the injury. These mechanisms include the disruption of the spinal cord blood barrier, edema and ion imbalance, in particular intracellular calcium and sodium concentrations, glutamate excitotoxicity, free radicals, and the inflammatory response contributing to the neurodegenerative process which is characterized by demyelination and apoptosis of neuronal tissue.

scholarly journals IL-1β-induces NF-κB and upregulates microRNA-372 to inhibit spinal cord injury recovery

2017 ◽  
Vol 117 (6) ◽  
pp. 2282-2291 ◽  
Author(s):  
Wei Zhou ◽  
Tongzhou Yuan ◽  
Youshui Gao ◽  
Peipei Yin ◽  
Wei Liu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Stem Cell ◽  
Functional Recovery ◽  
Neuronal Damage ◽  
Critical Role ◽  
Myeloperoxidase Activity ◽  
Cell Transplant ◽  
Tissue Water ◽  
Cord Injury

Excessive inflammation including IL-1β-initiated signaling is among the earlies reactions that can cause neuronal damage following spinal cord injury (SCI). It has been suggested that microRNAs may participate in stem cell repair to facilitate functional recovery following SCI. In this study we have shown that in cultured human neural stem cells (hNSC), IL-1β reduced the expression of both KIF3B (kinesin family member 3B) and NOSIP (nitric oxide synthase-interacting protein), two key modulators for restricting inflammation and promoting neuronal regeneration. The induction of microRNA-372 (miR-372) by IL-1β is specifically responsible for the inhibition of KIF3B and NOSIP. The 3′-untranslated regions (UTRs) of both KIF3B and NOSIP contain targeting sequences to miR-372 that directly inhibit their expression. Moreover, we found that the expression of miR-372 was stimulated in hNSC by IL-1β through an NF-κB binding site at its promoter region. Finally, stable overexpression of miR-372 inhibitor in hNSC rescued the IL-1β-induced impairment as shown by significant improvements in tissue water content, myeloperoxidase activity, and behavioral assessments in SCI rats. These findings suggest a critical role of miR-372 in inflammatory signaling and pinpoint a novel target for the treatment of acute SCI. NEW & NOTEWORTHY Our data demonstrate that IL-1β can impair the functional recovery of neural stem cell transplant therapy for spinal cord injury (SCI) treatment in rats. This effect is dependent on microRNA-372 (miR-372)-dependent gene repression of KIF3B and NOSIP. Therefore, specific knockdown of miR-372 may provide benefits for SCI treatments.

scholarly journals The Complement Receptor C5aR Controls Acute Inflammation and Astrogliosis following Spinal Cord Injury

2015 ◽  
Vol 35 (16) ◽  
pp. 6517-6531 ◽  
Author(s):  
F. H. Brennan ◽  
R. Gordon ◽  
H. W. Lao ◽  
P. J. Biggins ◽  
S. M. Taylor ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Acute Inflammation ◽  
Complement Receptor ◽  
Cord Injury

scholarly journals Effect of Shikonin on Spinal Cord Injury in Rats Via Regulation of HMGB1/TLR4/NF-kB Signaling Pathway

2017 ◽  
Vol 43 (2) ◽  
pp. 481-491 ◽  
Author(s):  
Yihui Bi ◽  
Yapeng Zhu ◽  
Mingkai Zhang ◽  
Keke Zhang ◽  
Xingyi Hua ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Motor Function ◽  
Tissue Repair ◽  
Underlying Mechanism ◽  
Molecular Signaling ◽  
Cord Injury

Background/Aims: Shikonin, a compound extracted from Zicao, has been demonstrated to hold anti-bacterial, anti-inflammatory, and anti-tumor activities in various diseases and it has been shown to protect human organs from injuries. However, the effect of shikonin on the recovery of spinal cord injury (SCI) remains unknown. This study was designed to estimate the potential therapeutic effect and underlying mechanism of shikonin on SCI in vivo. Methods: In the study, we used HE staining, ELISA assay, transfection assay, TUNEL assay, real time PCR and Western blot to detect the effects of shikonin on spinal cord injury in rats. Results: we showed that shikonin could promote the recovery of motor function and tissue repair after SCI treatment in rats SCI model. Moreover, we demonstrated that shikonin inhibited the spinal cord edema in SCI model of rats. According to further investigation, shikonin induced the reduction of inflammatory response through decreasing the expression levels of HMGB1, TLR4 and NF-κB after SCI injury. In addition, we also found that shikonin could suppress the apoptosis and expression of caspase-3 protein in SCI model of rats. Conclusion: Our results demonstrated that shikonin induced the recovery of tissue repair and motor function via inactivation of HMGB1/TLR4/NF-κB signaling pathway in SCI model of rats. Meanwhile, shikonin regulated the inflammation response in SCI by suppressing the HMGB1/TLR4/NF-κB signaling pathway. The described mechanism sheds novel light on molecular signaling pathway in spinal cord injury and secondary injury including inflammatory response.

scholarly journals A Canine's Behavior and Cognitive State as It Relates to Immobility and the Success of Physical Rehabilitation in the Non-ambulatory Spinal Cord Patient

2021 ◽  
Vol 8 ◽  
Author(s):  
Stephanie A. Thomovsky ◽  
Niwako Ogata
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Physical Therapists ◽  
Critical Role ◽  
Physical Rehabilitation ◽  
Psychological State ◽  
Cognitive State ◽  
Injury Rehabilitation ◽  
Cardiopulmonary Fitness ◽  
Cord Injury

Physical rehabilitation (PR) is recommended following spinal cord injury to help improve and maintain muscle elasticity, joint mobility, and nerve health. It can also be used to relieve pain and improve cardiopulmonary fitness in an immobile patient. There is evidence, in human medicine, that PR plays a critical role in mental health and the psychological state of the patient. As part of the assessment phase, human physical therapists often identify psychosocial symptoms and barriers at the start of PR that ultimately may affect improvement in human patients suffering from injury and the loss of mobility. Patient psychological state plays an integral role in healing and outcome during treatment and rehabilitation. Specific interventions set to address these symptoms can better outcome. Arguably, one of the most emotionally traumatizing injuries suffered by a canine patient can be immobility secondary to spinal cord injury. Poorly understood is the role the canine cognitive state plays in the success of rehabilitation following spinal cord injury. Should breed, age, sex, physical fitness, personality, previous experiences and history or home lifestyle, affect the PR assessment of these patients? Do these factors affect eventual outcome following PR? The purpose of this manuscript is to explore psychosocial barriers encountered during injury rehabilitation in humans and determine if the similar barriers need to be considered when assessing a canine patient for spinal cord injury rehabilitation.

Critical role of microglia in the inflammatory response after spinal injury

2015 ◽  
Vol 3 (3) ◽  
pp. 453-462
Author(s):  
Ya-Yun Shi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Responses ◽  
Spinal Injury ◽  
Critical Role ◽  
Cell Types ◽  
Inflammatory Factors ◽  
Cytokines And Chemokines ◽  
Cord Injury

Spinal cord injury induces a robust neuroinflammatory response that includes marked changes in the variety of endogenous CNS cell types specially microglia. In response to spinal injury, microglia undergo dramatic changes in cell morphology and promote inflammatory responses, which result in production of inflammatory factors and oxidative stress including reactive oxygen species. Further pro-inflammatory cytokines and chemokines are also rapidly up-regulated and likely contribute to microglial activation. This topic review will explore the current research on microglial responses to spinal injury and the recent progress in the pharmacologic and molecular targeting of microglia in spinal injury. Finally, we explore the argument for a positive versus negative role of microglia after spinal cord injury.

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