scholarly journals Transfer RNA-Derived Fragments and isomiRs Are Novel Components of Chronic TBI-Induced Neuropathology

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 136
Author(s):  
Noora Puhakka ◽  
Shalini Das Das Gupta ◽  
Niina Vuokila ◽  
Asla Pitkänen
Keyword(s):  
Traumatic Brain Injury ◽  
Messenger Rna ◽  
Transfer Rna ◽  
Secondary Injury ◽  
Behavioral Outcome ◽  
Chronic Neuroinflammation ◽  
Non Coding Rna ◽  
Differentially Expressed Mirnas ◽  
The Brain ◽  
Small Rnaseq

Neuroinflammation is a secondary injury mechanism that evolves in the brain for months after traumatic brain injury (TBI). We hypothesized that an altered small non-coding RNA (sncRNA) signature plays a key role in modulating post-TBI secondary injury and neuroinflammation. At 3threemonths post-TBI, messenger RNA sequencing (seq) and small RNAseq were performed on samples from the ipsilateral thalamus and perilesional cortex of selected rats with a chronic inflammatory endophenotype, and sham-operated controls. The small RNAseq identified dysregulation of 2 and 19 miRNAs in the thalamus and cortex, respectively. The two candidates from the thalamus and the top ten from the cortex were selected for validation. In the thalamus, miR-146a-5p and miR-155-5p levels were upregulated, and in the cortex, miR-375-3p and miR-211-5p levels were upregulated. Analysis of isomiRs of differentially expressed miRNAs identified 3′nucleotide additions that were increased after TBI. Surprisingly, we found fragments originating from 16 and 13 tRNAs in the thalamus and cortex, respectively. We further analyzed two upregulated fragments, 3′tRF-IleAAT and 3′tRF-LysTTT. Increased expression of the full miR-146a profile, and 3′tRF-IleAAT and 3′tRF-LysTTT was associated with a worse behavioral outcome in animals with chronic neuroinflammation. Our results highlight the importance of understanding the regulatory roles of as-yet unknown sncRNAs for developing better strategies to treat TBI and neuroinflammation.

scholarly journals LINC01018 and SMIM25 sponged miR-182-5p in endometriosis revealed by the ceRNA network construction

2020 ◽  
Vol 34 ◽  
pp. 205873842097630
Author(s):  
Li Jiang ◽  
Mengmeng Zhang ◽  
Sixue Wang ◽  
Yuzhen Xiao ◽  
Jingni Wu ◽  
...  
Keyword(s):  
Messenger Rna ◽  
Kegg Pathway ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Differentially Expressed ◽  
Protein Protein Interaction ◽  
Cerna Network ◽  
Non Coding Rna ◽  
Differentially Expressed Mirnas ◽  
Long Non Coding Rna

The current study intended to explore the interaction of the long non-coding RNA (lncRNA), microRNA (miRNA), and messenger RNA (mRNA) under the background of competitive endogenous RNA (ceRNA) network in endometriosis (EMs). The differentially expressed miRNAs (DEmiRs), differentially expressed lncRNA (DELs), and differentially expressed genes (DEGs) between EMs ectopic (EC) and eutopic (EU) endometrium based on three RNA-sequencing datasets (GSE105765, GSE121406, and GSE105764) were identified, which were used for the construction of ceRNA network. Then, DEGs in the ceRNA network were performed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) analysis. Besides, the DEmiRs in the ceRNA network were validated in GSE124010. And the target DELs and DEGs of verified DEmiRs were validated in GSE86534. The correlation of verified DEmiRs, DEGs, and DELs was explored. Moreover, gene set enrichment analysis (GSEA) was applied to investigate the function of verified DEmiRs, DEGs, and DELs. Overall, 1352 DEGs and 595 DELs from GSE105764, along with 27 overlapped DEmiRs between GSE105765 and GSE121406, were obtained. Subsequently, a ceRNA network, including 11 upregulated and 16 downregulated DEmiRs, 7 upregulated and 13 downregulated DELs, 48 upregulated and 46 downregulated DEGs, was constructed. The GO and KEGG pathway analysis showed that this ceRNA network probably was associated with inflammation-related pathways. Furthermore, hsa-miR-182-5p and its target DELs (LINC01018 and SMIM25) and DEGs (BNC2, CHL1, HMCN1, PRDM16) were successfully verified in the validation analysis. Besides, hsa-miR-182-5p was significantly negatively correlated with these target DELs and DEGs. The GSEA analysis implied that high expression of LINC01018, SMIM25, and CHL1, and low expression of hsa-miR-182-5p would activate inflammation-related pathways in endometriosis EU samples. LINC01018 and SMIM25 might sponge hsa-miR-182-5p to upregulate downstream genes such as CHL1 to promote the development of endometriosis.

scholarly journals Screening of Biochemical and Molecular Mechanisms of Secondary Injury and Repair in the Brain after Experimental Blast-Induced Traumatic Brain Injury in Rats

2013 ◽  
Vol 30 (11) ◽  
pp. 920-937 ◽  
Author(s):  
Patrick M. Kochanek ◽  
C. Edward Dixon ◽  
David K. Shellington ◽  
Samuel S. Shin ◽  
Hülya Bayır ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Molecular Mechanisms ◽  
Secondary Injury ◽  
Injury And Repair ◽  
The Brain

scholarly journals Paternal chronic folate supplementation induced the transgenerational inheritance of acquired developmental and metabolic changes in chickens

2019 ◽  
Vol 286 (1910) ◽  
pp. 20191653 ◽  
Author(s):  
Shengru Wu ◽  
Wei Guo ◽  
Xinyi Li ◽  
Yanli Liu ◽  
Yulong Li ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Messenger Rna ◽  
Metabolic Changes ◽  
Micro Rna ◽  
Differentially Expressed ◽  
Folate Supplementation ◽  
Non Coding Rna ◽  
Differentially Expressed Mirnas ◽  
Long Non Coding Rna ◽  
Competitive Endogenous Rna

Increasing evidence indicates that paternal diet can result in metabolic changes in offspring, but the definite mechanism remains unclear in birds. Here, we fed breeder cocks five different diets containing 0, 0.25, 1.25, 2.50 and 5.00 mg kg −1 folate throughout life. Paternal folate supplementation (FS) was beneficial to the growth and organ development of broiler offspring. Most importantly, the lipid and glucose metabolism of breeder cocks and broiler offspring were affected by paternal FS, according to biochemical and metabolomic analyses. We further employed global analyses of hepatic and spermatozoal messenger RNA (mRNA), long non-coding RNA (lncRNA) and micro RNA (miRNA). Some key genes involved in the glycolysis or gluconeogenesis pathway and the PPAR signalling pathway, including PEPCK , ANGPTL4 and THRSP , were regulated by differentially expressed hepatic and spermatozoal miRNAs and lncRNAs in breeder cocks and broiler offspring. Moreover, the expression of ANGPTL4 could also be regulated by differentially expressed miRNAs and lncRNAs in spermatozoa via competitive endogenous RNA (ceRNA) mechanisms. Overall, this model suggests that paternal folate could transgenerationally regulate lipid and glucose metabolism in broiler offspring and the epigenetic transmission may involve altered spermatozoal miRNAs and lncRNAs.

scholarly journals Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1

2021 ◽  
Vol 12 ◽  
Author(s):  
Colleen N. Bodnar ◽  
James B. Watson ◽  
Emma K. Higgins ◽  
Ning Quan ◽  
Adam D. Bachstetter
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Immune Cells ◽  
Interleukin 1 ◽  
Brain Lesion ◽  
The Body ◽  
Future Research ◽  
Secondary Injury ◽  
Inflammatory Regulation ◽  
The Brain

Several barriers separate the central nervous system (CNS) from the rest of the body. These barriers are essential for regulating the movement of fluid, ions, molecules, and immune cells into and out of the brain parenchyma. Each CNS barrier is unique and highly dynamic. Endothelial cells, epithelial cells, pericytes, astrocytes, and other cellular constituents each have intricate functions that are essential to sustain the brain’s health. Along with damaging neurons, a traumatic brain injury (TBI) also directly insults the CNS barrier-forming cells. Disruption to the barriers first occurs by physical damage to the cells, called the primary injury. Subsequently, during the secondary injury cascade, a further array of molecular and biochemical changes occurs at the barriers. These changes are focused on rebuilding and remodeling, as well as movement of immune cells and waste into and out of the brain. Secondary injury cascades further damage the CNS barriers. Inflammation is central to healthy remodeling of CNS barriers. However, inflammation, as a secondary pathology, also plays a role in the chronic disruption of the barriers’ functions after TBI. The goal of this paper is to review the different barriers of the brain, including (1) the blood-brain barrier, (2) the blood-cerebrospinal fluid barrier, (3) the meningeal barrier, (4) the blood-retina barrier, and (5) the brain-lesion border. We then detail the changes at these barriers due to both primary and secondary injury following TBI and indicate areas open for future research and discoveries. Finally, we describe the unique function of the pro-inflammatory cytokine interleukin-1 as a central actor in the inflammatory regulation of CNS barrier function and dysfunction after a TBI.

Head trauma: treatment and diagnostic aids

2020 ◽  
Vol 25 (11) ◽  
pp. 283-288
Author(s):  
Mark Lowrie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Best Practice ◽  
Treatment Options ◽  
Brain Parenchyma ◽  
Primary Lesion ◽  
Trauma Treatment ◽  
Secondary Injury ◽  
Irreversible Damage ◽  
The Brain

Traumatic brain injury occurs frequently in dogs and cats. The primary lesion occurs at the time of injury and causes direct, irreversible damage to the brain parenchyma and vasculature. Secondary lesions occur in the minutes following the trauma as a result of a combination of physical and biochemical changes that lead to intracranial hypertension. It is this secondary injury that veterinarians are able to reduce. This article outlines the treatment options for patients with traumatic brain injury. There remains controversy over what constitutes best practice. This article addresses the main points regarding the clinical therapeutic options currently available.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

Providing Care of Mild Traumatic Brain Injury by the Family Practice/Primary Care Optometrist

2018 ◽  
pp. 110-119
Keyword(s):  
Primary Care ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Family Practice ◽  
Advanced Training ◽  
Entry Level ◽  
The Family ◽  
Basic Understanding ◽  
The Brain

Primary Objectives: By extending the scope of knowledge of the primary care optometrist, the brain injury population will have expanded access to entry level neurooptometric care by optometric providers who have a basic understanding of their neurovisual problems, be able to provide some treatment and know when to refer to their colleagues who have advanced training in neuro-optometric rehabilitation.

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