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Condition: Spinal Cord Injury
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Total 126 results found since Jan 2013.
Up-regulation of TRAF2 Suppresses Neuronal Apoptosis after Rat Spinal Cord Injury.
In this study, we detected the dynamic change patterns of TRAF2 expression using an acute spinal cord contusion (SCC) model in adult rats. Western blot analysis and immunohistochemistry identified significant upregulation of TRAF2 after SCI. Double-immunofluorescent staining demonstrated that the upregulated TRAF2 was found predominantly in neurons. Moreover, colocalization of TRAF2 with active caspase-3/-8 was detected in NeuN-positive cells. In vitro, we analyzed the association of TRAF2 with active caspase-3/8 on PC12 cells by western blot analysis, which paralleled the in vivo data. Knockdown ofTRAF2 with siRNA demonst...
Source: Tissue and Cell - August 16, 2017 Category: Cytology Authors: Xu G, Zhang J, Wang L, Cui Z, Sun X, Liu Z, Zhu Z, Qiu Y Tags: Tissue Cell Source Type: research
lncRNA-Map2k4 sequesters miR-199a to promote FGF1 expression and spinal cord neuron growth.
Abstract
Spinal cord injury (SCI) is a common critical illness in clinical practice. SCI prevention, treatment and rehabilitation have become important topics in today's medical profession. Studies have shown that long noncoding RNAs (lncRNAs) also play an important role in the pathology of SCI. The biology software analysis identified miR-199a binding sites in the lncRNA-Map2k4 and FGF1 sequences, which were confirmed by the subsequent dual luciferase reporter assay. When lncRNA-Map2k4 expression was down-regulated by siRNA, miR-199a expression in neurons was up-regulated and FGF1 expression was down-regulated. I...
Source: Biochemical and Biophysical Research communications - June 24, 2017 Category: Biochemistry Authors: Lv HR Tags: Biochem Biophys Res Commun Source Type: research
MiR-25 protects PC-12 cells from H2O2 mediated oxidative damage via WNT/ β-catenin pathway.
CONCLUSIONS: miR-25 protects PC-12 cells against H2O2-induced oxidative damage though regulation of Nrf2 and activation of Wnt/β-catenin and PI3 K/AKT/ERK signaling.
PMID: 28605990 [PubMed - as supplied by publisher]
Source: Journal of Spinal Cord Medicine - June 15, 2017 Category: Orthopaedics Tags: J Spinal Cord Med Source Type: research
Targeted siRNA delivery reduces nitric oxide mediated cell death after spinal cord injury
Traumatic spinal cord injury (SCI) includes the primary insult as well as a sequela of biochemical and cellular cascades that amplifies the initial injury. This degenerative process, known as secondary injury,...
Source: Journal of Nanobiotechnology - May 8, 2017 Category: Nanotechnology Authors: Wen Gao and Jianming Li Source Type: research
Α‐synuclein induces microglial cell migration through stimulating HIF‐1α accumulation
Microglial cell migration and infiltration plays a critical role in spinal cord injury after thoracoabdominal aortic surgery. In our previous study, α‐synuclein, a presynaptic protein was shown to be released from injured neurons and cause microglial cell activation. Here, we aimed to explore the effect of α‐synuclein on microglial cell migration. Primary microglial cells were isolated from Sprague–Dawley rats and then exposed different doses (0.2, 0.4, and 0.6 μM) of α‐synuclein oligomers. The mRNA and protein levels of HIF‐1α were then analyzed by qRT‐PCR and Western blot. Cell migration was examined b...
Source: Journal of Neuroscience Research - January 30, 2017 Category: Neuroscience Authors: Hongfei Qiao, Xijing He, Qiaojun Zhang, Ni Zhang, Libo Li, Yanping Hui, Wenjuan Li, Dong Wang, Zhonghen Wu Tags: Research Article Source Type: research
The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis.
In this study, we have performed an acute SCI model in adult rats and investigated the dynamic changes of IGFBP6 expression in the spinal cord. Our results showed that IGFBP6 was upregulated significantly after SCI, which was paralleled with the levels of apoptotic proteins p53 and active caspase-3. Immunofluorescent labeling showed that IGFBP6 was co-localizated with active caspase-3 and p53 in neurons. To further investigate the function of IGFBP6, an apoptosis model was established in primary neuronal cells. When IGFBP6 was knocked down by specific short interfering RNA (siRNA), the protein levels of active caspase-3 an...
Source: Neurochemical Research - November 25, 2016 Category: Neuroscience Authors: Wang S, Liu Y, Wu C, Zhao W, Zhang J, Bao G, Xu G, Sun Y, Chen J, Cui Z Tags: Neurochem Res Source Type: research
Curcumin inhibits glial scar formation by suppressing astrocyte-induced inflammation and fibrosis in vitro and in vivo.
This study confirmed that cur could regulate both the NF-κb and SOX9 signaling pathways and reduce the expression of intracellular and extracellular glial scar components through dual-target regulating both inflammation and fibrosis after SCI in the rat. This study provides an important hypothesis centered on the dual inhibition of intracellular and extracellular glial scar components as a treatment strategy for SCI.
PMID: 27865778 [PubMed - as supplied by publisher]
Source: Brain Research - November 15, 2016 Category: Neurology Authors: Yuan J, Liu W, Zhu H, Chen Y, Zhang X, Li L, Chu W, Wen Z, Feng H, Lin J Tags: Brain Res Source Type: research
NFAT5 protects astrocytes against oxygen –glucose–serum deprivation/restoration damage via the SIRT1/Nrf2 pathway
In this study, our aim is to investigate whether NFAT5 overexpression can protect astrocytes against oxygen –glucose–serum deprivation/restoration (OGSD/R) damage. In vivo, rats were subjected to ischemia–reperfusion injury, resulting in increased water content, infarct volume, and expression of NFAT5 protein in rat spinal cord. After primary culture for spinal cord astrocytes, the in vitro OGSD/R m odel was established. The results of the CCK8 assay and flow cytometry showed that, in the OGSD/R group, astrocyte cell viability was downregulated, but astrocyte apoptosis increased. Caspase 3 activity increased as well....
Source: Journal of Molecular Neuroscience - November 11, 2016 Category: Neuroscience Source Type: research
TWEAK-Fn14 Influences Neurogenesis Status via Modulating NF- κB in Mice with Spinal Cord Injury
In conclusion, stimulating the TWEAK-Fn14 pathway may elevate the expression of NF-κB, thereby slow the function recovery of SCI mice whereas inhibiting the TWEAK-Fn14 pathway may improve the neurogenesis status in mice with spinal cord injuries.
Source: Molecular Neurobiology - November 6, 2016 Category: Neurology Source Type: research
Contribution of the Suppressor of Variegation 3-9 Homolog 1 in Dorsal Root Ganglia and Spinal Cord Dorsal Horn to Nerve Injury –induced Nociceptive Hypersensitivity
Conclusions The findings of this study suggest that SUV39H1 contributes to nerve injury –induced allodynia and hyperalgesia through gating MOR expression in the injured DRG. SUV39H1 may be a potential target for the therapeutic treatment of nerve injury–induced nociceptive hypersensitivity.
Source: Anesthesiology - September 20, 2016 Category: Anesthesiology Source Type: research
Annexin A10 is involved in the development and maintenance of neuropathic pain in mice
We examined the gene expressions of the L5 spinal cord after spinal nerve ligation (SNL)-induced neuropathic pain in mice by gene chip. The results showed that Anxa10 mRNA was the most upregulated gene in annexin family with 73.7-fold increase. Although previous studies have reported that several annexins are involved in nociceptive pain, the role of Anxa10 in pain remains undefined. We aimed to evaluate the role of ANXA10 in mediating injury-induced heat hyperalgesia and mechanical allodynia. We found that SNL induced persistent upregulation of Anxa10 mRNA and protein in the spinal cord of mice. Moreover, ANXA10 was coloc...
Source: Neuroscience Letters - August 9, 2016 Category: Neuroscience Source Type: research
Nanoparticle-Delivered IRF5 siRNA Facilitates M1 to M2 Transition, Reduces Demyelination and Neurofilament Loss, and Promotes Functional Recovery After Spinal Cord Injury in Mice
ABSTRACT
Macrophage activation and persistent inflammation contribute to the pathogenesis of spinal cord injury (SCI), and different phenotypes of macrophages play diverse roles in the pathological process of SCI. After SCI, there is an acute phase of alternatively activated (M2) macrophage infiltration, followed by a long-lasting phase of classically activated (M1) macrophage accumulation in the wound. The long-lasting predominance of M1 macrophages may derail healing and compromise organ functions. Based on the previous findings that the transcription factor interferon regulatory factor 5 (IRF5) up-regulates gen...
Source: Inflammation - July 18, 2016 Category: Allergy & Immunology Source Type: research
Role of Nectin-1/c-Src Signaling in the Analgesic Effect of GDNF on a Rat Model of Chronic Constrictive Injury
In this study, we aimed to examine whether the adhesion protein nectin-1 and its downstream protein c-Src are involved in neuropathic pain. We found that nectin-1 was expressed in the superficial dorsal horn of the spinal cord and that it was increased after chronic constrictive injury (CCI). Intrathecal administration of nectin-1 siRNA attenuated neuropathic pain induced by CCI via interference of the expression of nectin-1. Furthermore, we found that GDNF can downregulate the phosphorylation level of nectin-1-associated c-Src without changing the expression level of nectin-1. In summary, these data suggest that nectin-1 ...
Source: Journal of Molecular Neuroscience - July 8, 2016 Category: Neuroscience Source Type: research
Temporal and Spatial Expression of LGR5 After Acute Spinal Cord Injury in Adult Rats.
In this study, we examined LGR5 expression and cellular localization in rats following acute SCI. Western blot analysis and immunohistochemistry exhibited an important upregulation of LGR5 in injury spinal cord. Double immunofluorescence staining showed that LGR5 was co-expressed with glial fibrillary acidic protein (GFAP). Moreover, we detected that PCNA had colocalization with LGR5 and GFAP after SCI. In the vitro model, we could find the enhanced expression of LGR5 in the primary astrocyte which was induced by the lipopolysaccharide (LPS). In particular, we found the significantly decreased ability for proliferation whe...
Source: Neurochemical Research - June 22, 2016 Category: Neuroscience Authors: Chen X, Hao J, Fu T, Liu J, Yu M, He S, Qian R, Zhang F Tags: Neurochem Res Source Type: research
