Disease of mRNA Regulation: Relevance for Ischemic Brain Injury

DeGracia, Donald J.

doi:10.1007/s12975-017-0586-7

Cited by 8 publications

(6 citation statements)

References 64 publications

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“…Thus, mitochondrial transfer would be efficient to rescue damaged cells in crisis, compared with other relatively timeconsuming approaches that promote mitochondrial biosynthesis. In addition to the neuroprotective approaches identified in the animal models of ischemic stroke [13][14][15][16], mitochondrial transfer reveals a new neuroprotective mechanism of stem cell therapy against ischemic stroke.…”

Section: Introductionmentioning

confidence: 99%

Stem Cell Therapy in Brain Ischemia: The Role of Mitochondrial Transfer

Huang

Reis

Boling

et al. 2020

Stem Cells and Development

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Mitochondrial dysfunction is an important pathological process in the setting of ischemic brain injury. Stem cell-mediated mitochondrial transfer provides an efficient intercellular process to supply additional mitochondria in the ischemic brain tissues. In this review, we summarize the mitochondrial pathology associated with brain ischemia, mechanisms of stem cell-mediated mitochondrial transfer, and in vitro/in vivo experimental findings of mitochondrial transfer from stem cells to ischemic vascular endothelial cells/neurons as potential therapeutic strategy in the management of ischemic brain injury.

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Section: Introductionmentioning

confidence: 99%

Stem Cell Therapy in Brain Ischemia: The Role of Mitochondrial Transfer

Huang

Reis

Boling

et al. 2020

Stem Cells and Development

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“…Our REACTOME pathway and PANTHER process enrichment analyses performed on all markers including miRNA levels revealed the strong impact of translation, RNA, metabolism of mRNA, RNA splicing, and nonsense-mediated decay on the interactome of death due to IS, indicating that dysfunctions in postischemic translation regulation are involved. During ischemia and brain cell injury, translation may arrest due to lack of ATP, and changes in translational regulation at the mRNA level and the ribosomic network may develop, which may cause a multitude of aberrations in the downstream PPI and metabolic network modules [143,144]. The nonsense-mediated decay pathway degrades transcripts with a premature stop codon, thereby reducing errors in gene expression.…”

Section: Interactions Pathways and Functions Which Bridge The Immune And Hemostasis Subdomainsmentioning

confidence: 99%

New Drug Targets to Prevent Death Due to Stroke: A Review Based on Results of Protein-Protein Interaction Network, Enrichment, and Annotation Analyses

Maes

Nikiforov

Plaimas

et al. 2021

IJMS

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This study used established biomarkers of death from ischemic stroke (IS) versus stroke survival to perform network, enrichment, and annotation analyses. Protein-protein interaction (PPI) network analysis revealed that the backbone of the highly connective network of IS death consisted of IL6, ALB, TNF, SERPINE1, VWF, VCAM1, TGFB1, and SELE. Cluster analysis revealed immune and hemostasis subnetworks, which were strongly interconnected through the major switches ALB and VWF. Enrichment analysis revealed that the PPI immune subnetwork of death due to IS was highly associated with TLR2/4, TNF, JAK-STAT, NOD, IL10, IL13, IL4, and TGF-β1/SMAD pathways. The top biological and molecular functions and pathways enriched in the hemostasis network of death due to IS were platelet degranulation and activation, the intrinsic pathway of fibrin clot formation, the urokinase-type plasminogen activator pathway, post-translational protein phosphorylation, integrin cell-surface interactions, and the proteoglycan-integrin extracellular matrix complex (ECM). Regulation Explorer analysis of transcriptional factors shows: (a) that NFKB1, RELA and SP1 were the major regulating actors of the PPI network; and (b) hsa-mir-26-5p and hsa-16-5p were the major regulating microRNA actors. In conclusion, prevention of death due to IS should consider that current IS treatments may be improved by targeting VWF, the proteoglycan-integrin-ECM complex, TGF-β1/SMAD, NF-κB/RELA and SP1.

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“…Our REACTOME pathway and PANTHER process enrichment analyses performed on all markers including miRNA levels revealed the strong impact of translation, RNA, metabolism of mRNA, RNA splicing, and nonsense mediated decay on the interactome of death due to IS, indicating that dysfunctions in post-ischemic translation regulation are involved. During ischemia and brain cell injury, translation may arrest due to lack of ATP and changes in translational regulation at the mRNA level and the ribosomic network may develop which may cause a multitude of aberrations in the downstream PPI and metabolic network modules [143,144]. The nonsense-mediated decay pathway degrades transcripts with premature stop codon thereby reducing errors in gene expression.…”

Section: Interactions Pathways and Functions Which Bridge The Immune And Hemostasis Subdomainsmentioning

confidence: 99%

New Drug Targets to Prevent Death due to Stroke: Results of Protein-Protein Interaction Network, Enrichment and Annotation Analyses.

Maes¹,

Nikiforov²,

Plaimas³

et al. 2021

Preprint

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This study used established biomarkers of death due to ischemic stroke (IS) and performed network, enrichment, and annotation analysis. Protein-protein interaction (PPI) network analysis revealed that the backbone of the highly connective network of IS death consisted of IL6, ALB, TNF, SERPINE1, VWF, VCAM1, TGFB1, and SELE. Cluster analysis revealed immune and hemostasis subnetworks, which were strongly interconnected through the major switches ALB and VWF. Enrichment analysis revealed that the PPI immune subnetwork of death due to IS was highly associated with TLR2/4, TNF, JAK-STAT, NOD, IL10, IL13, IL4, and TGF-β1/SMAD pathways. The top biological and molecular functions and pathways enriched in the hemostasis network of death due IS were platelet degranulation and activation, the intrinsic pathway of fibrin clot formation, the urokinase-type plasminogen activator pathway, post-translational protein phosphorylation, integrin cell surface interactions, and the proteoglycan-integrin-extra cellular matrix complex (ECM). Regulation Explorer analysis of transcriptional factors shows: a) that NFKB1, RELA and SP1 were the major regulating actors of the PPI network; and b) hsa-mir-26-5p and hsa-16-5p were the major regulating microRNA actors. In conclusion, prevention of death due to IS should consider that current IS treatments may be improved by targeting VWF, VEGFA, proteoglycan-integrin-ECM complex, NFKB/RELA and SP1.

show abstract

Disease of mRNA Regulation: Relevance for Ischemic Brain Injury

Cited by 8 publications

References 64 publications

Stem Cell Therapy in Brain Ischemia: The Role of Mitochondrial Transfer

Stem Cell Therapy in Brain Ischemia: The Role of Mitochondrial Transfer

New Drug Targets to Prevent Death Due to Stroke: A Review Based on Results of Protein-Protein Interaction Network, Enrichment, and Annotation Analyses

New Drug Targets to Prevent Death due to Stroke: Results of Protein-Protein Interaction Network, Enrichment and Annotation Analyses.

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