Differential expression of metabolic genes essential for glucose and lipid metabolism in skeletal muscle from spinal cord injured subjects

2011 ◽  
Vol 110 (5) ◽  
pp. 1204-1210 ◽  
Author(s):  
Yun Chau Long ◽  
Emil Kostovski ◽  
Hanneke Boon ◽  
Nils Hjeltnes ◽  
Anna Krook ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Mrna Levels ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury ◽  
The Impact ◽  
Spinal Cord Injured

Skeletal muscle plays an important role in the regulation of energy homeostasis; therefore, the ability of skeletal muscle to adapt and alter metabolic gene expression in response to changes in physiological demands is critical for energy balance. Individuals with cervical spinal cord lesions are characterized by tetraplegia, impaired thermoregulation, and altered skeletal muscle morphology. We characterized skeletal muscle metabolic gene expression patterns, as well as protein content, in these individuals to assess the impact of spinal cord injury on critical determinants of skeletal muscle metabolism. Our results demonstrate that mRNA levels and protein expression of skeletal muscle genes essential for glucose storage are reduced, whereas expression of glycolytic genes is reciprocally increased in individuals with spinal cord injury. Furthermore, expression of genes essential for lipid oxidation is coordinately reduced in spinal cord injured subjects, consistent with a marked reduction of mitochondrial proteins. Thus spinal cord injury resulted in a profound and tightly coordinated change in skeletal muscle metabolic gene expression program that is associated with the aberrant metabolic features of the tissue.

233-LB: Spinal Cord Injury Inhibited-FGF21 Signaling Is Associated with Dysregulation of Metabolic Gene Expression in Mouse Liver and Adipose Tissue

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 233-LB
Author(s):  
XIN-HUA LIU ◽  
LAUREN HARLOW ◽  
ZACHARY GRAHAM ◽  
JOSHUA F. YARROW ◽  
KENNETH CUSI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adipose Tissue ◽  
Mouse Liver ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury

scholarly journals Spinal Cord Injury Increases Pro-inflammatory Cytokine Expression in Kidney at Acute and Sub-chronic Stages

Inflammation ◽  
2021 ◽  
Author(s):  
Shangrila Parvin ◽  
Clintoria R. Williams ◽  
Simone A. Jarrett ◽  
Sandra M. Garraway
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Inflammatory Cytokine ◽  
Cardiovascular Health ◽  
Mrna Levels ◽  
Post Injury ◽  
Cord Injury ◽  
And Function ◽  
The Impact

Abstract— Accumulating evidence supports that spinal cord injury (SCI) produces robust inflammatory plasticity. We previously showed that the pro-inflammatory cytokine tumor necrosis factor (TNF)α is increased in the spinal cord after SCI. SCI also induces a systemic inflammatory response that can impact peripheral organ functions. The kidney plays an important role in maintaining cardiovascular health. However, SCI-induced inflammatory response in the kidney and the subsequent effect on renal function have not been well characterized. This study investigated the impact of high and low thoracic (T) SCI on C-fos, TNFα, interleukin (IL)-1β, and IL-6 expression in the kidney at acute and sub-chronic timepoints. Adult C57BL/6 mice received a moderate contusion SCI or sham procedures at T4 or T10. Uninjured mice served as naïve controls. mRNA levels of the proinflammatory cytokines IL-1β, IL-6, TNFα, and C-fos, and TNFα and C-fos protein expression were assessed in the kidney and spinal cord 1 day and 14 days post-injury. The mRNA levels of all targets were robustly increased in the kidney and spinal cord, 1 day after both injuries. Whereas IL-6 and TNFα remained elevated in the spinal cord at 14 days after SCI, C-fos, IL-6, and TNFα levels were sustained in the kidney only after T10 SCI. TNFα protein was significantly upregulated in the kidney 1 day after both T4 and T10 SCI. Overall, these results clearly demonstrate that SCI induces robust systemic inflammation that extends to the kidney. Hence, the presence of renal inflammation can substantially impact renal pathophysiology and function after SCI.

Gene expression profiling of experimental traumatic spinal cord injury as a function of distance from impact site and injury severity

2005 ◽  
Vol 22 (3) ◽  
pp. 368-381 ◽  
Author(s):  
Andrea De Biase ◽  
Susan M. Knoblach ◽  
Simone Di Giovanni ◽  
Chenguang Fan ◽  
Annamaria Molon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Injury Severity ◽  
Comprehensive Evaluation ◽  
Gene Clusters ◽  
Functional Class ◽  
Impact Site ◽  
Cord Injury ◽  
The Impact

Changes in gene expression contribute to pathophysiological alterations following spinal cord injury (SCI). We examined gene expression over time (4 h, 24 h, 7 days) at the impact site, as well as rostral and caudal regions, following mild, moderate, or severe contusion SCI in rats. High-density oligonucleotide microarrays were used that included ∼27,000 genes/ESTs (Affymetrix RG-U34; A, B and C arrays), together with multiple analyses (MAS 5.0, dChip). Alterations after mild injury were relatively rapid (4 and 24 h), whereas they were delayed and prolonged after severe injury (24 h and 7 days). The number and magnitude of gene expression changes were greatest at the injury site after moderate injury and increased in rostral and caudal regions as a function of injury severity. Sham surgery resulted in expression changes that were similar to mild injury, suggesting the importance of using time-linked surgical controls as well as naive animals for these kinds of studies. Expression of many genes and ESTs was altered; these were classified functionally based on ontology. Overall representation of these functional classes varied with distance from the site of injury and injury severity, as did the individual genes that contributed to each functional class. Different clustering approaches were used to identify changes in neuronal-specific genes and several transcription factors that have not previously been associated with SCI. This study represents the most comprehensive evaluation of gene expression changes after SCI to date. The results underscore the power of microarray approaches to reveal global genomic responses as well as changes in particular gene clusters and/or families that may be important in the secondary injury cascade.

scholarly journals Influence of Different ECM-Like Hydrogels on Neurite Outgrowth Induced by Adipose Tissue-Derived Stem Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
E. Oliveira ◽  
R. C. Assunção-Silva ◽  
O. Ziv-Polat ◽  
E. D. Gomes ◽  
F. G. Teixeira ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Stem Cells ◽  
Spinal Cord Injury ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Growth Factors ◽  
Axonal Outgrowth ◽  
Mrna Levels ◽  
Cord Injury

Mesenchymal stem cells (MSCs) have been proposed for spinal cord injury (SCI) applications due to their capacity to secrete growth factors and vesicles—secretome—that impacts important phenomena in SCI regeneration. To improve MSC survival into SCI sites, hydrogels have been used as transplantation vehicles. Herein, we hypothesized if different hydrogels could interact differently with adipose tissue-derived MSCs (ASCs). The efficacy of three natural hydrogels, gellan gum (functionalized with a fibronectin peptide), collagen, and a hydrogel rich in laminin epitopes (NVR-gel) in promoting neuritogenesis (alone and cocultured with ASCs), was evaluated in the present study. Their impact on ASC survival, metabolic activity, and gene expression was also evaluated. Our results indicated that all hydrogels supported ASC survival and viability, being this more evident for the functionalized GG hydrogels. Moreover, the presence of different ECM-derived biological cues within the hydrogels appears to differently affect the mRNA levels of growth factors involved in neuronal survival, differentiation, and axonal outgrowth. All the hydrogel-based systems supported axonal growth mediated by ASCs, but this effect was more robust in functionalized GG. The data herein presented highlights the importance of biological cues within hydrogel-based biomaterials as possible modulators of ASC secretome and its effects for SCI applications.

scholarly journals Fosl1 Targets AMPK to Inhibit Autophagy-Mediated Anti-Apoptotic and Anti-Inflammatory Effects in Spinal Cord Injury

2020 ◽  
Author(s):  
Lin Zhong ◽  
Sheng Fang ◽  
An-Quan Wang ◽  
Tao Wang ◽  
Wei Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Animal Model ◽  
Inflammatory Factor ◽  
Mrna Levels ◽  
Ampk Activation ◽  
Cord Injury ◽  
Anti Inflammatory

Abstract Background: The objective of this study was to delineate the role of Fosl1 in regulating inflammation and apoptosis following spinal cord injury.Methods: GSE45006 datasets from Gene Expression Omnibus (GEO) were explored to analyze Fosl1 gene expression. Next, we established an animal model to assess Fosl1 and AMPK by western blotting, real-time PCR, and immunohistochemical staining and used immunofluorescence staining to check Fosl1 expression in neurons. Fosl1 silencing was used to assess the effect on AMPK, cell viability, autophagy, inflammation and apoptosis. Subsequently, an AMPK activator and inhibitor were added to PC-12 cells with H2O2-induced injury subjected to si-Fosl1 treatment to examine the change in the above indexes and to determine whether the benefits from Fosl1 silencing occurred via AMPK. Moreover, we employed chloroquine (CQ) and rapamycin (RAP) to activate and inhibit autophagy, respectively, and revealed the effects of the upregulation and downregulation of autophagy following AMPK interference. Finally, an animal model was used to identify the effect of si-Fosl1 in vivo.Results: Based on the analysis of the GSE45006 datasets, Fosl1 was found to be highly expressed and was also found to be significantly enhanced in our animal model. Fosl1 knockdown upregulated AMPK at the protein and mRNA levels, promoted autophagic proteins (LC3 II/I, Beclin1) and inhibited inflammatory factors (IL-1β, IL-6, TNF-α) and apoptosis markers (caspase3, Bax). However, Fosl1 decreased the negatively related autophagic protein p62, the anti-inflammatory factor IL-10 and the anti-apoptotic marker Bcl-2. By utilizing compound C (com, an AMPK inhibitor), we learned that AMPK inhibition exhibited unfavorable effects on autophagy but promoted inflammation and apoptosis following Fosl1 silencing. AMPK activation showed contrasting effects. Moreover, we used CQ (an autophagic inhibitor), which indicated that CQ reversed the benefits of AMPK activation on inflammation and apoptosis. The autophagic activator RAP attenuated the negative effects after com treatment. In vivo, si-Fosl1 increased BBB scores at 7 d and 14 d and motor neurons, meanwhile, it decreased the number of apoptotic cells, and inflammatory cytokine expression at 14 d postoperation. Conclusion: Fosl1 can suppress AMPK to promote inflammation and apoptosis through autophagy in SCI.

Gene Expression Profiling Of Skeletal Muscle After Spinal Cord Injury

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S35
Author(s):  
Karen L. Riska ◽  
Yi-Wen Chen ◽  
Patrick Lee ◽  
Francis Lee ◽  
Maria L. Urso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Cord Injury

scholarly journals The Influence of Social Support on the Lived Experiences of Spinal Cord Injured Sportsmen

2003 ◽  
Vol 17 (2) ◽  
pp. 135-156 ◽  
Author(s):  
Tim Rees ◽  
Brett Smith ◽  
Andrew C. Sparkes
Keyword(s):  
Social Support ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Lived Experiences ◽  
Positive Influence ◽  
Life History Data ◽  
Cord Injury ◽  
Tangible Support ◽  
The Impact ◽  
Spinal Cord Injured

This study draws upon life history data to investigate the influence of social support on the lives of 6 men who had acquired a spinal cord injury and become disabled through playing sport. Interviews were analyzed utilizing categorical-content analysis (Lieblich, Tuval-Mashiach, & Zilber, 1998). The participants experienced emotional, esteem, informational, and tangible support (Rees & Hardy, 2000) from various sources. Alongside the positive influence of social support, examples are shown of inappropriate or negatively-experienced support and where participants considered sport to be lacking. The spinal cord injured person is encouraged to be proactive in resourcing social support, but providers might also be taught to recognize the impact, either positively or negatively, that their giving support can have.

Gene Expression Profiling Of Skeletal Muscle After Spinal Cord Injury

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S35
Author(s):  
Karen L. Riska ◽  
Yi-Wen Chen ◽  
Patrick Lee ◽  
Francis Lee ◽  
Maria L. Urso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Cord Injury

scholarly journals Noninvasive determination of inspiratory pressure in patients with spinal cord injury: what is the best method?

2009 ◽  
Vol 35 (3) ◽  
pp. 256-260
Author(s):  
Andrea Ponte Rocha ◽  
Sergio Ricardo Menezes Mateus ◽  
Thomas Anthony Horan ◽  
Paulo Sérgio Siebra Beraldo
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inspiratory Pressure ◽  
Cord Injury ◽  
Impaired Pulmonary Function ◽  
Injured Patients ◽  
The Impact ◽  
Spinal Cord Injured ◽  
Sniff Nasal Inspiratory Pressure

The aim of the study was to evaluate the performance of sniff nasal inspiratory pressure (SNIP) and MIP in individuals with spinal cord injury. We evaluated 26 patients with spinal cord injury. Mean FVC in those with tetraplegia was 52 ± 19% of predicted, compared with 78 ± 23% of predicted in those with paraplegia (p < 0.05). In contrast, the percentage of predicted SNIP was lower in those with tetraplegia than in those with paraplegia (p < 0.05). In all participants, SNIP correlated significantly with the level of the injury (r = 0.489; 95% CI: 0.125-0.737). The impact that the greater discriminatory power of SNIP has on the diagnosis of impaired pulmonary function in spinal cord-injured patients should be investigated further.

scholarly journals Impact of short- and long-term electrically induced muscle exercise on gene signaling pathways, gene expression, and PGC1a methylation in men with spinal cord injury

2020 ◽  
Vol 52 (2) ◽  
pp. 71-80
Author(s):  
Michael A. Petrie ◽  
Arpit Sharma ◽  
Eric B. Taylor ◽  
Manish Suneja ◽  
Richard K. Shields
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Specific Gene ◽  
Muscle Exercise ◽  
Gene Sets ◽  
Cord Injury ◽  
Key Pathways

Exercise attenuates the development of chronic noncommunicable diseases (NCDs). Gene signaling pathway analysis offers an opportunity to discover if electrically induced muscle exercise regulates key pathways among people living with spinal cord injury (SCI). We examined short-term and long-term durations of electrically induced skeletal muscle exercise on complex gene signaling pathways, specific gene regulation, and epigenetic tagging of PGC1a, a major transcription factor in skeletal muscle of men with SCI. After short- or long-term electrically induced exercise training, participants underwent biopsies of the trained and untrained muscles. RNA was hybridized to an exon microarray and analyzed by a gene set enrichment analysis. We discovered that long-term exercise training regulated the Reactome gene sets for metabolism (38 gene sets), cell cycle (36 gene sets), disease (27 gene sets), gene expression and transcription (22 gene sets), organelle biogenesis (4 gene sets), cellular response to stimuli (8 gene sets), immune system (8 gene sets), vesicle-mediated transport (4 gene sets), and transport of small molecules (3 gene sets). Specific gene expression included: oxidative catabolism of glucose including PDHB ( P < 0.001), PDHX ( P < 0.001), MPC1 ( P < 0.009), and MPC2 ( P < 0.007); Oxidative phosphorylation genes including SDHA ( P < 0.006), SDHB ( P < 0.001), NDUFB1 ( P < 0.002), NDUFA2 ( P < 0.001); transcription genes including PGC1α ( P < 0.030) and PRKAB2 ( P < 0.011); hypertrophy gene MSTN ( P < 0.001); and the myokine generating FNDC5 gene ( P < 0.008). Long-term electrically induced exercise demethylated the major transcription factor PGC1a. Taken together, these findings support that long-term electrically induced muscle activity regulates key pathways associated with muscle health and systemic metabolism.

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