Pediatric Research, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 26, 2024
Language: Английский
Biomolecules, Journal Year: 2024, Volume and Issue: 14(10), P. 1307 - 1307
Published: Oct. 16, 2024
Neutrophil extracellular traps (NETs) are intricate, DNA-based, web-like structures adorned with cytotoxic proteins. They play a crucial role in antimicrobial defense but also implicated autoimmune diseases and tissue injury. The process of NET formation, known as NETosis, is regulated cell death mechanism that involves the release these unique to neutrophils. NETosis heavily dependent on production reactive oxygen species (ROS), which can be generated either through NADPH oxidase (NOX) or mitochondrial pathways, leading NOX-dependent NOX-independent respectively. Recent research has revealed an intricate interplay between ROS production, DNA repair, formation different contexts. UV radiation trigger combined apoptosis, apoNETosis, driven by repair. Similarly, calcium ionophore-induced both repair key components, only partial role. In case bacterial infections, early stages pivotal. Interestingly, serum-free conditions, spontaneous occurs NOX-derived ROS, early-stage inhibition halting process, while late-stage increases it. balance processes appears critical factor regulating pathways being activated depending nature stimulus. These findings not deepen our understanding mechanisms behind suggest potential therapeutic targets for conditions where NETs contribute disease pathology.
Language: Английский
Citations
11
Frontiers in Medicine, Journal Year: 2024, Volume and Issue: 10
Published: Jan. 12, 2024
Neutrophil extracellular traps (NETs) are essential for immune defense and have been increasingly recognized their role in infection inflammation. In the context of airway inflammatory diseases, there is growing evidence suggesting involvement significance NETs. This review aims to provide an overview formation mechanisms components NETs impact on various including acute lung injury/ARDS, asthma, chronic obstructive pulmonary disease (COPD) cystic fibrosis. By understanding inflammation, we can gain valuable insights into underlying pathogenesis these diseases identify potential targets future therapeutic strategies that either target or modulate harmful effects. Further research warranted elucidate complex interactions between inflammation develop targeted therapies effectively mitigate detrimental effects while preserving beneficial functions host defense.
Language: Английский
Citations
6
Neurosurgery Clinics of North America, Journal Year: 2025, Volume and Issue: 36(2), P. 113 - 126
Published: Feb. 5, 2025
Language: Английский
Citations
0
International Journal of Neuroscience, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 14
Published: Feb. 7, 2025
Previous studies have shown that an increased number of immune cells is closely associated with the onset and course changes intracerebral hemorrhage, but exact causal relationship has not been clarified. The aim this study was to investigate between hemorrhage by a two-way Mendelian randomization method. Two sets SNPs were used as instrumental variables analyses performed leave-one-out method assess validity heterogeneity included genetic variation instruments. level multiplicity variance instruments assessed. results showed clear three no related while scatterplot funnel plot confirmed causality less likely be biased; MR-Egger suggested pleiotropy found. Leave-one-out analysis applied suggest MR for single SNP robust; meanwhile, Meta-analysis combine two datasets, in fixed-effects model random-effects model, immunocyte CD66b on Granulocytic Myeloid-Derived Suppressor Cells other significantly causally test there significant difference different datasets. present found specific cell phenotypes analysis.
Language: Английский
Citations
0
Frontiers in Neurology, Journal Year: 2025, Volume and Issue: 16
Published: Feb. 28, 2025
Background Apoptosis plays a significant role in secondary brain injury following intracerebral hemorrhage (ICH). Currently, the mechanisms related to cell apoptosis after cerebral are still under investigation. Methods We identified differentially expressed genes (DEGs) between human ICH patients and normal individuals from GEO database conducted GO KEGG functional enrichment analyses on these DEGs. then constructed PPI network used MECDE algorithm identify key potentially involved ICH. Additionally, we miRNAs that might regulate apoptotic an mRNA-miRNA interaction network. Finally, validated bioinformatics results rat model. Results In model, 645 DEGs were identified. indicated primarily immune response, inflammatory apoptosis. GSEA analysis showed of process. By comparing with apoptosis-related MSigDB database, 110 among Further MOCDE revealed BID be gene ICH, which was within model The interactions construction suggested miR1225-3p may important miRNA regulating expression Conclusion critical regulation serves as biomarker process hemorrhage.
Language: Английский
Citations
0
Brain Hemorrhages, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
Language: Английский
Citations
0
Neurobiology of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 106936 - 106936
Published: May 1, 2025
Aging is an independent predictor of adverse outcomes after intracerebral hemorrhage (ICH), a stroke subtype with no effective treatment. Despite the expected increase in incidence ICH due to population aging and widespread use anticoagulants, preclinical studies aged animal subjects are lacking, pathophysiology has yet be defined. Herein, we attempt determine brain proteomic changes using unbiased label- free quantitative proteomics approach bioinformatics. To this end, male female mice (18-24 months old) were subjected sham/ICH. Mice euthanized on day 3 post-surgery, ipsilateral tissue was collected LC-MS/MS analysis. Considering sex as biological variable, data derived from males females separately analyzed. The analysis revealed 133 differentially expressed proteins (DEPs) between sham groups subjects. Among DEPs, 98 downregulated, 35 upregulated ICH, compared sham. In mice, 315 DEPs identified, which 221 94 mass spectrometry validated immunohistochemistry or western blot analysis, bioinformatics comprehensive understanding signaling pathways associated ICH. Some both that could play roles pathology 14-3-3 S100-A9. study also mitochondrial dysfunction critical regulator ICH-induced acute damage. Overall, generated help develop hypothesis-driven functional delineate complex pathobiology
Language: Английский
Citations
0
Phytomedicine, Journal Year: 2024, Volume and Issue: 128, P. 155438 - 155438
Published: Feb. 19, 2024
Yi-Qi-Huo-Xue Decoction (YQHXD), a traditional Chinese medicine formula, has demonstrated efficacy in the clinical treatment of intracerebral hemorrhage (ICH) for over decade. Nevertheless, precise pharmacotherapeutic compounds YQHXD capable penetrating into cerebral tissue and pharmacological underpinnings remain ambiguous. The active components rat brains was analyzed by ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry. potential targets, pathways biological progresses ameliorating ICH induced injury predicted network pharmacology. Moreover, collagenase-induced model, primary cortex neurons exposed to hemin molecular docking were applied validate mechanisms YQHXD. Eleven identified within brains. Employing Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) databases, our investigation concentrated on roles autophagy BDNF/TrkB signaling pathway context. results revealed that alleviated neurological dysfunction, brain water content, swelling, pathological caused ICH. Meanwhile, inhibited influx autophagosome vivo, regulated neuronal TrkB/BDNF both vivo vitro. Subsequently, N-acetyl serotonin (NAS), selective TrkB agonist, employed corroborate significance this process. combination NAS did not further enhance protective rats. Additionally, outcomes analysis nine exhibited regulatory effects TrkB. Ipsilateral activated 72 h after effectively resisted ICH, which related suppression ipsilateral via pathway. This study provides novel insights therapeutic context treatment.
Language: Английский
Citations
3
Materials Today Bio, Journal Year: 2024, Volume and Issue: 28, P. 101218 - 101218
Published: Aug. 24, 2024
Traumatic spinal cord injury (SCI) always leads to severe neurological deficits and permanent damage. Neuroinflammation is a vital process of SCI have become promising target for treatment. However, the neuroinflammation-targeted therapy would hinder functional recovery lead treatment failure. Herein, biomimic anti-neuroinflammatory nanoplatform (DHCNPs) was developed active neutrophil extracellular traps (NETs) targeting The curcumin-loaded liposome with anti-inflammatory property acted as core DHCNPs. Platelet membrane were fused form hybrid DHCNPs hijacking neutrophils neutralizing elevated neutrophil-related proinflammatory cytokines, respectively. DNAse I modification on could achieve NETs degradation, blood barrier, neuron repair. Further studies proved that reprogram multifaceted neuroinflammation reverse via nuclear factor kappa-B (NF-κB) pathway. We believe current study provides new perspective inhibition may shed light SCI.
Language: Английский
Citations
2
Translational Stroke Research, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 28, 2024
Perihematomal edema (PHE) significantly aggravates secondary brain injury in patients with intracerebral hemorrhage (ICH), yet its detailed mechanisms remain elusive. Neutrophil extracellular traps (NETs) are known to exacerbate neurological deficits and worsen outcomes after stroke. This study explores the potential role of NETs pathogenesis following ICH. The rat ICH model was created, immunofluorescence Western blot were used examine neutrophil accumulation, NET markers citrullinated histone H3 (CitH3) myeloperoxidase (MPO), tight junction proteins (ZO-1 Occludin), Aquaporin-4 (AQP4), matrix metalloproteinase-9 (MMP-9), ERK phosphorylation (p-ERK) tissues surrounding hematoma. TUNEL staining behavioral tests employed evaluate neuronal apoptosis dysfunction, while blood-brain barrier (BBB) permeability also measured by Evans blue water content. Furthermore, molecular related NETs-induced PHE investigated using NETs, ERK, MMP-9 AQP4 regulators, respectively. Ly6G+ neutrophils hematoma developed within 3 days post-ICH. decreased proteins, destroyed BBB integrity, promoted edema, increased apoptosis, exacerbated deficits. Conversely, inhibition mitigated PHE, reduced improved functions. Mechanistically, NET-induced originated from impairment via ERK/MMP9 pathway, coupled ERK-mediated downregulation perihematomal regions. These findings elucidated effects on which offered promising insights for targeting relieve
Language: Английский
Citations
2