Medium-chain Fatty Acids as Biomarkers of Mitochondrial Dysfunction in Traumatic Brain Injury

González‐Domínguez, Raúl

doi:10.1016/j.ebiom.2016.09.024

Cited by 8 publications

(14 citation statements)

References 10 publications

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“…Although severe TBI is one of the main causes of death or disability in patients, mild or moderate TBI is a leading cause of long-term disability including seizures and emotional and behavioural issues [2]. The damage to the cranium and the intracranial contents caused by a TBI can be divided into the primary injury and delayed secondary injury, which is more profound and includes axonal shearing [3], neuroinflammation [4,5], neurochemical changes [6,7], brain edema [8], vascular injury [9], cell apoptosis [10] and mitochondrial dysfunction [11].…”

Section: Introductionmentioning

confidence: 99%

Plasma Exosome-derived MicroRNAs as Novel Biomarkers of Traumatic Brain Injury in Rats

Wang

Zhang

et al. 2020

Int. J. Med. Sci.

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Traumatic brain injury (TBI) is a widespread central nervous system (CNS) condition and a leading cause of death, disability, and long-term disability including seizures and emotional and behavioral issues. To date, applicable diagnostic biomarkers have not been elucidated. MicroRNAs (miRNAs) are enriched and stable in exosomes in plasma. Therefore, we speculated that miRNAs in plasma exosomes might serve as novel biomarkers for TBI diagnosis and are also involved in the pathogenesis of TBI. In this study, we first isolated exosomes from peripheral blood plasma in rats with TBI and then investigated the alterations in miRNA expression in exosomes by high-throughput RNA sequencing. As a result, we identified 50 significantly differentially expressed miRNAs, including 31 upregulated and 19 downregulated miRNAs. Then, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the most highly correlated pathways that were identified were the MAPK signaling pathway, regulation of actin cytoskeleton, Rap1 signaling pathway and Ras signaling pathway. This study provides novel perspectives on miRNAs in peripheral blood plasma exosomes, which not only could be used as biomarkers of TBI diagnosis but could also be manipulated as therapeutic targets of TBI.

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Section: Introductionmentioning

confidence: 99%

Plasma Exosome-derived MicroRNAs as Novel Biomarkers of Traumatic Brain Injury in Rats

Wang

Zhang

et al. 2020

Int. J. Med. Sci.

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“…The characterization of the release of these specific metabolites during the metabolic changes could clarify the pathophysiology and the potential therapeutic targets. Several metabolic biomarkers of acute TBI have been proposed, including S100 calcium binding protein B (S100B) [ 15 – 18 ], glial fibrillary acidic protein (GFAP) [ 19 ], neuron-specific enolase (NSE) [ 20 , 21 ], sphingolipid (SPL) [ 22 ], and medium-chain fatty acids [ 23 ]. However, a single biomarker is of limited utility for revealing the mechanism and developing therapeutic strategies in TBI treatment.…”

Section: Introductionmentioning

confidence: 99%

Plasma metabolomics profiles in rats with acute traumatic brain injury

et al. 2017

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Traumatic brain injury (TBI) is a major cause of mortality and disability worldwide. We validated the utility of plasma metabolomics analysis in the clinical diagnosis of acute TBI in a rat model of controlled cortical impact (CCI) using gas chromatography/mass spectrometry (GC/MS). Thirty Sprague-Dawley rats were randomly divided into two groups of 15 rats each: the CCI group and sham group. Blood samples were obtained from the rats within the first 24 h after TBI injury. GC/MS measurements were performed to evaluate the profile of acute TBI-induced metabolic changes, resulting in the identification of 45 metabolites in plasma. Principal component analysis, partial least squares-discriminant analysis, orthogonal partial least square discriminant analysis using hierarchical clustering and univariate/multivariate analyses revealed clear differences in the plasma metabolome between the acute CCI group and the sham group. CCI induced distinctive changes in metabolites including linoleic acid metabolism, amino acid metabolism, galactose metabolism, and arachidonic acid metabolism. Specifically, the acute CCI group exhibited significant alterations in proline, phosphoric acid, β-hydroxybutyric acid, galactose, creatinine, L-valine, linoleic acid and arachidonic acid. A receiver operating characteristic curve analysis showed that the above 8 metabolites in plasma could be used as the potential biomarkers for the diagnosis of acute TBI. Furthermore, this study is the first time to identify the galactose as a biomarker candidate for acute TBI. This comprehensive metabolic analysis complements target screening for potential diagnostic biomarkers of acute TBI and enhances predictive value for the therapeutic intervention of acute TBI.

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“…In the same way, cytochrome C is released, which will bind with the activation factor of the apoptotic protease (Apaf-1) and ATP to form a protein complex called apoptosome. [2][3][4] These apoptosomes adhere to caspase-activating proteins. The direct initiation of apoptotic mechanisms arises from the activation of the first signaling process of apoptosis ligand and tumor necrosis factor (TNF), which is the main extrinsic mediator of apoptosis activated by macrophages.…”

Section: Role Of Inflammatory Responsementioning

confidence: 99%

“…2,4,11 The phospholipids of their membranes play an important role in cell structure and survival using a role in the moderation of cell proliferation as programmed cell death. [3][4][5] At the cellular level, mitochondria modulate transmembrane potential, cellular thermal regulation and calcium storage, 1,4 an essential component in bioenergy, and cellular function; they also have the task of maintaining the homeostasis of neuronal cells through a variety of intricate processes, such as autophagy, the elimination of compounds and harmful elements of metabolism, in response to a variety of metabolic demands that include the stress associated to ROS. 4,9…”

Section: Role Of Mitochondria In Tbimentioning

confidence: 99%

“…The high morbidity and mortality are mainly due to the lack of effective diagnoses and treatments despite the intensive care strategies for these patients. 1 An important limitation for a successful outcome is the lack of understanding of the underlying complex and dynamic cellular and molecular events, the characterization of a cascade of biochemical and pathophysiological reactions, 2,3 emphasizing mitochondrial dysfunction, key to investigate more deeply about this pathology in the search of possible biomarkers that allow an opportune diagnosis, stratification of the severity, monitoring, and prognosis, with this identifying possible complications, and the opportunity to establish better strategies before these cases. 3 This article will review the cellular processes that are performed after a TBI, specifically in the mechanisms of mitochondrial dysfunction, the way in which they affect the course of the disease, and the measures currently used in this situation.…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial Dysfunction in Traumatic Brain Injury: Management Strategies

Bonilla-Mendoza

García-Ballestas

Pacheco-Hernández

et al. 2020

Indian Journal of Neurotrauma

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Today, traumatic brain injuries continue to be studied, increasingly investigating the pathophysiological mechanisms that contribute to the clinical presentation, severity, and possible sequelae, but despite this, the prognosis of these patients is sometimes poor. Mitochondrial dysfunction comprises a series of reactions that contribute to the inflammatory process in these patients that have an impact on the prognosis, since it is one of the pathophysiological mechanisms involved in secondary lesions after a traumatic brain injury; and therefore has opened a field of study in the search of possible biomolecular markers that allow us to establish a prognosis and prediction of mortality.

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Medium-chain Fatty Acids as Biomarkers of Mitochondrial Dysfunction in Traumatic Brain Injury

Cited by 8 publications

References 10 publications

Plasma Exosome-derived MicroRNAs as Novel Biomarkers of Traumatic Brain Injury in Rats

Plasma Exosome-derived MicroRNAs as Novel Biomarkers of Traumatic Brain Injury in Rats

Plasma metabolomics profiles in rats with acute traumatic brain injury

Mitochondrial Dysfunction in Traumatic Brain Injury: Management Strategies

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