The rising roles of exosomes in the tumor microenvironment reprogramming and cancer immunotherapy

MedComm, Год журнала: 2024, Номер 5(4)

Опубликована: Апрель 1, 2024

Abstract Exosomes are indispensable for intercellular communications. Tumor microenvironment (TME) is the living environment of tumor cells, which composed various components, including immune cells. Based on TME, immunotherapy has been recently developed eradicating cancer cells by reactivating antitumor effect The communications between and TME crucial development, metastasis, drug resistance. play an important role in mediating these regulating reprogramming affects sensitivity immunotherapy. Therefore, it imperative to investigate exosomes impact Here, we review communication remodeling efficacy immunotherapy, as well summarize underlying mechanisms. Furthermore, also introduce potential application artificially modified delivery systems drugs. Further efforts this field will provide new insights roles progression, thus helping us uncover effective strategies treatment.

Язык: Английский

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Electrochemical detection of extracellular vesicles for early diagnosis: a focus on disease biomarker analysis

Extracellular Vesicles and Circulating Nucleic Acids, Год журнала: 2024, Номер 5(2), С. 165 - 79

Опубликована: Апрель 28, 2024

This review article presents a detailed examination of the integral role that electrochemical detection extracellular vesicles (EVs) plays, particularly focusing on potential application for early disease diagnostics through EVs biomarker analysis. Through an exploration benefits and challenges presented by vetted protein, lipid, nucleic acid analysis, we underscore significance these techniques. Evidence from recent studies renders this modality imperative in identifying diverse biomarkers EVs, leading to diagnosis diseases such as cancer neurodegenerative disorders. Recent advancements have led enhanced sensitivity, specificity point-of-care testing (POCT) are elucidated, along with equipment deployed detection. The concludes contemplation future perspectives, recognizing shifts prognosis, necessary advances broad adoption, areas ongoing research. objective is propel further investigation into rapidly burgeoning field, thereby facilitating paradigm shift detection, monitoring, treatment toward human health management.

Язык: Английский

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The cGAS/STING signaling pathway is involved in sevoflurane induced neuronal necroptosis via regulating microglia M1 polarization

Cellular Signalling, Год журнала: 2024, Номер 119, С. 111195 - 111195

Опубликована: Апрель 28, 2024

The specific mechanisms of sevoflurane-induced neurotoxicity are still undetermined. aim the current study was to investigate role cyclic GMP-AMP synthase (cGAS)-stimulator interferon genes (STING) signaling pathway in neuronal necroptosis.

Язык: Английский

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Propofol improves sleep deprivation‐induced sleep structural and cognitive deficits via upregulating the BMAL1 expression and suppressing microglial M1 polarization

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(7)

Опубликована: Июль 1, 2024

Abstract Background Sleep deprivation (SD) is a growing global health problem with many deleterious effects, such as cognitive impairment. Microglia activation‐induced neuroinflammation may be an essential factor in this. Propofol has been shown to clear sleep debt after SD rats. This study aims evaluate the effects of propofol‐induced on ameliorating quality impairment and decline 48 h SD. Methods Almost 8–12‐week‐old rats were placed system for natural or continuous Afterwards, received propofol (20 mg·kg −1 ·h , 6 h) via tail slept naturally. The Morris water maze (MWM) Y‐maze test assessed spatial learning memory abilities. Rat EEG/EMG monitored sleep. expression brain muscle Arnt‐like protein 1 (BMAL1), brain‐derived neurotrophic (BDNF) hippocampus BMAL1 hypothalamus by western blot. Enzyme‐linked immunosorbent assay detected IL‐6, IL‐1β, arginase (Arg1), IL‐10 levels hippocampus. Immunofluorescence was used determine microglia well morphological changes. Results Compared control group, sleep‐deprived showed poor performance both MWM test, accompanied disturbances structure, including increased total time, time spent delta power non‐rapid eye movement In addition, induces abnormal circadian rhythm BMAL1, activates microglia, causes nerve damage. reversed these changes saved Furthermore, treatment significantly reduced hippocampal IL‐1β IL‐6 levels, BDNF, Arg1, switched surface markers from inflammatory M1 type anti‐inflammatory M2 type. Conclusion reduces SD‐induced disruption, possibly lowering neuronal inflammation switching phenotype activated state, thus exerting neuroprotective effects.

Язык: Английский

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circHOMER1 Alleviates Sevoflurane‐Induced Hippocampal Neuronal Injury via Targeted Negative Regulation of miR‐217

Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(1)

Опубликована: Янв. 1, 2025

ABSTRACT Sevoflurane (Sev) is a widely applied anesthetic in clinical practice; however, it could induce neurotoxicity and lead to postoperative cognitive dysfunction (POCD). This study aimed investigate the role underlying mechanism of circHOMER1 Sev‐induced POCD. Sev treated mouse hippocampal neuronal HT22 cells SD rats. RT‐qPCR was used detect levels miR‐217. ELISA employed measure inflammatory factors IL‐6, IL‐1β, TNF‐α. Commercially available kits assessed concentration MDA measured activities LDH SOD. The CCK‐8 assay cell viability. Flow cytometry analyzed apoptosis. Morris water maze test evaluated learning abilities Dual luciferase reporter assays RIP experiments validated targeted binding treatment significantly reduces viability, increases apoptosis, stimulates responses oxidative stress, induces memory impairments Following exposure Sev, expression markedly decreased, while overexpression can alleviate neuroinflammation, deficits CircHOMER1 targets miR‐217, transfection miR‐217 antagonizes neuroprotective effects circHOMER1. demonstrated that negatively regulated thereby inhibiting disorders.

Язык: Английский

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TNF-α Enhanced Activity of Sympathetic Neurons in Superior Cervical Ganglion to Promote Chronic Sleep Deprivation-Related Hyperalgesia

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 24, 2025

Язык: Английский

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Impact of Microglia-Derived Extracellular Vesicles on Resident Central Nervous System Cell Populations After Acute Brain Injury Under Various External Stimuli Conditions

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Март 24, 2025

Acute brain injuries (ABI) caused by various emergencies can lead to structural and functional damage tissue. Common causes include traumatic injury, cerebral hemorrhage, ischemic stroke, heat stroke. Globally, ABI represent a significant portion of neurosurgical cases. Previous studies have emphasized the therapeutic potential stem cell-derived extracellular vesicles (EVs). Recent research indicates that EVs extracted from resident cells in central nervous system (CNS) also show following injury. Microglia, as innate immune CNS, respond changes internal environment altering their phenotype secreting impact CNS cells, including neurons, astrocytes, oligodendrocytes, endothelial neural (NSCs), microglia themselves. Notably, under different external stimuli, either promote neuronal survival, angiogenesis, myelin regeneration while reducing glial scarring inflammation, or they exert opposite effects. This review summarizes evaluates current findings on how microglia-derived influence after stimuli. It analyzes interaction mechanisms between discusses future directions clinical applications.

Язык: Английский

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Anesthesia-mediated neuroinflammatory sequelae in post operative cognitive dysfunction: mechanisms and therapeutic implications

Frontiers in Anesthesiology, Год журнала: 2024, Номер 3

Опубликована: Фев. 27, 2024

Post-operative cognitive dysfunction (POCD) is an iatrogenic decline with unclear etiology. While current hypotheses include surgical and pharmacological-induced neuroinflammatory mechanisms, the growing prevalence, especially amongst geriatric population, emphasizes ambiguity of dysfunction. Recent studies have highlighted potential role general regional anesthesia in pathogenesis POCD; these pharmacological effects been demonstrated to disrupt blood-brain barrier integrity, influence microglial polarization, linked worsening prognoses decline. Moreover, mechanical stress from intervention reperfusion injury may exacerbate generation reactive oxygen species (ROS), thereby increasing oxidative brain synergistically disruptions. In previous studies, factors for variable incidence various risk explored. this review, we examine local, regional, on molecular cellular glial response, along its intercellular interactions previously reported clinical outcomes.

Язык: Английский

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The NF-κB Pathway: Key Players in neurocognitive functions and related disorders

European Journal of Pharmacology, Год журнала: 2024, Номер 984, С. 177038 - 177038

Опубликована: Окт. 5, 2024

Язык: Английский

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The miR-182-5p/GPX4 Pathway Contributes to Sevoflurane-Induced Ototoxicity via Ferroptosis

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(12), С. 6774 - 6774

Опубликована: Июнь 20, 2024

Our study aimed to investigate the role of ferroptosis in sevoflurane-induced hearing impairment and explore mechanism microRNA-182-5p (miR-182-5p)/Glutathione Peroxidase 4 (GPX4) pathway ototoxicity. Immunofluorescence staining was performed using myosin 7a CtBP2. Cell viability assessed CCK-8 kit. Fe2+ concentration measured FerroOrange Mi-to-FerroGreen fluorescent probes. The lipid peroxide level BODIPY 581/591 C11 MitoSOX auditory brainstem response (ABR) test conducted evaluate status. Bioinformatics tools dual luciferase gene reporter analysis were used confirm direct targeting miR-182-5p on GPX4 mRNA. expression cells by qRT-PCR Western blot. Ferrostatin-1 (Fer-1) pretreatment significantly improved damage ribbon synapses mice caused sevoflurane exposure. revealed that Fer-1 reduced intracellular mitochondrial iron overload, as well accumulation. findings indicated upregulated sevoflurane-exposed HEI-OC1 cells, regulated binding 3′UTR inhibition attenuated overload elucidated miR-182-5p/GPX4 implicated ototoxicity promoting ferroptosis.

Язык: Английский

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