Role of regulatory non-coding RNAs in traumatic brain injury

Li, Shun; Qiu, Na; Ni, Andrew; Hamblin, Milton H.; Yin, Ke-Jie

doi:10.1016/j.neuint.2023.105643

Cited by 8 publications

(1 citation statement)

References 262 publications

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“…While serum lncRNA biomarkers for rmTBI have not been described previously, the role of lncRNAs in brain injury has been demonstrated. MALAT1, NEAT1, SNHG1, MEG3, HOTAIR were shown to be involved in inflammation angiogenesis, apoptosis and cell proliferation pathways in the brain, and their levels changed in the brain tissue in mouse models of TBI [73][74][75][76][77][78]. These studies did not measure circulating blood levels of lncRNA in mouse models of TBI.…”

Section: Discussionmentioning

confidence: 97%

Long Noncoding RNA VLDLR-AS1 Levels in Serum Correlate with Combat-Related Chronic Mild Traumatic Brain Injury and Depression Symptoms in US Veterans

Patel,

Krause-Hauch,

Kenney

et al. 2024

IJMS

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More than 75% of traumatic brain injuries (TBIs) are mild (mTBI) and military service members often experience repeated combat-related mTBI. The chronic comorbidities concomitant with repetitive mTBI (rmTBI) include depression, post-traumatic stress disorder or neurological dysfunction. This study sought to determine a long noncoding RNA (lncRNA) expression signature in serum samples that correlated with rmTBI years after the incidences. Serum samples were obtained from Long-Term Impact of Military-Relevant Brain-Injury Consortium Chronic Effects of Neurotrauma Consortium (LIMBIC CENC) repository, from participants unexposed to TBI or who had rmTBI. Four lncRNAs were identified as consistently present in all samples, as detected via droplet digital PCR and packaged in exosomes enriched for CNS origin. The results, using qPCR, demonstrated that the lncRNA VLDLR-AS1 levels were significantly lower among individuals with rmTBI compared to those with no lifetime TBI. ROC analysis determined an AUC of 0.74 (95% CI: 0.6124 to 0.8741; p = 0.0012). The optimal cutoff for VLDLR-AS1 was ≤153.8 ng. A secondary analysis of clinical data from LIMBIC CENC was conducted to evaluate the psychological symptom burden, and the results show that lncRNAs VLDLR-AS1 and MALAT1 are correlated with symptoms of depression. In conclusion, lncRNA VLDLR-AS1 may serve as a blood biomarker for identifying chronic rmTBI and depression in patients.

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Section: Discussionmentioning

confidence: 97%

Long Noncoding RNA VLDLR-AS1 Levels in Serum Correlate with Combat-Related Chronic Mild Traumatic Brain Injury and Depression Symptoms in US Veterans

Patel,

Krause-Hauch,

Kenney

et al. 2024

IJMS

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Transplantation of miR-193b-3p-Transfected BMSCs Improves Neurological Impairment after Traumatic Brain Injury through S1PR3-Mediated Regulation of the PI3K/AKT/mTOR Signaling Pathway

He,

Li,

Zhang

et al. 2024

Crit Rev Eukaryot Gene Expr

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The aim of the present study was to explore the molecular mechanisms by which miR-193b-3p-trans-fected bone marrow mesenchymal stem cells (BMSCs) transplantation improves neurological impairment after traumatic brain injury (TBI) through sphingosine-1-phosphate receptor 3 (S1PR3)-mediated regulation of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway at the cellular and animal levels. BMSCs were transfected with miR-193b-3p. A TBI cell model was established by oxygen-glucose deprivation (OGD)-induced HT22 cells, and a TBI animal model was established by controlled cortical impact (CCI). Cell apoptosis was detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL), and cell activity was detected by a cell counting kit 8 (CCK-8) assay. Western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expression of related proteins and genes. In this study, transfection of miR-193b-3p into BMSCs significantly enhanced BMSCs proliferation and differentiation. Transfection of miR-193b-3p reduced the levels of the interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-alpha (TNF-α) inflammatory factors in cells and mouse models, and it inhibited neuronal apoptosis, which alleviated OGD-induced HT22 cell damage and neural function damage in TBI mice. Downstream experiments showed that miR-193b-3p targeting negatively regulated the expression of S1PR3, promoted the activation of the PI3K/AKT/mTOR signaling pathway, and inhibited the levels of apoptosis and inflammatory factors, which subsequently improved OGD-induced neuronal cell damage and nerve function damage in TBI mice. However, S1PR3 overexpression or inhibition of the PI3K/AKT/mTOR signaling pathway using the IN-2 inhibitor weakened the protective effect of miR-193b-3p-transfected BMSCs on HT22 cells. Transplantation of miR-193b-3p-transfected BMSCs inhibits neurological injury and improves the progression of TBI in mice through S1PR3-mediated regulation of the PI3K/AKT/mTOR pathway.

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Research progress on digestive disorders following traumatic brain injury

Lin,

Hou,

Wang

et al. 2024

Front. Immunol.

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Traumatic brain injury (TBI) is a prevalent disease that poses a significant threat to global public health. Digestive dysfunction, as a common complication, is of particular importance to understand its pathogenesis, diagnostic criteria, and relevant treatment strategies. TBI can affect digestive function through inflammatory immune responses, the enteric nervous system, and hormonal levels. Furthermore, TBI can also impact neurologic recovery through bidirectional communication along the brain-gut axis. Therefore, this article aims to summarize the underlying mechanisms and further explore individualized feeding strategies, therapeutic approaches, long-term prognosis for TBI patients, as well as recent advancements in related technologies. Further understanding of the pathogenesis of digestive system dysfunction after TBI on the basis of the interaction of gut-brain axis is conducive to more future therapies to treat TBI and improve the long-term prognosis of patients through improving digestive function, and achieve good clinical efficacy.

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Role of regulatory non-coding RNAs in traumatic brain injury

Cited by 8 publications

References 262 publications

Long Noncoding RNA VLDLR-AS1 Levels in Serum Correlate with Combat-Related Chronic Mild Traumatic Brain Injury and Depression Symptoms in US Veterans

Long Noncoding RNA VLDLR-AS1 Levels in Serum Correlate with Combat-Related Chronic Mild Traumatic Brain Injury and Depression Symptoms in US Veterans

Transplantation of miR-193b-3p-Transfected BMSCs Improves Neurological Impairment after Traumatic Brain Injury through S1PR3-Mediated Regulation of the PI3K/AKT/mTOR Signaling Pathway

Research progress on digestive disorders following traumatic brain injury

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