Inflammatory stimulation of astrocytes affects the expression of miRNA-22-3p within NSCs-EVs regulating remyelination by targeting KDM3A

Han, Tianyu; Song, Peiwen; Wu, Zuomeng; Wang, Cancan; Liu, Yunlei; Wang, Ying; Li, Kaixuan; Shen, Cailiang

doi:10.1186/s13287-023-03284-w

Cited by 10 publications

(6 citation statements)

References 71 publications

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“…miRNAs are one of these regulatory factors. Currently, there are increasing reports on the study of miRNAs regulating the biological characteristics of NSCs [35][36][37][38] .…”

Section: Resultsmentioning

confidence: 99%

The Impact of microRNA-29a-3p on the Neural Stem Cell Differentiation Process into Neurons

Shi,

Zhou,

Dai

et al. 2023

IJPS

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Shi et al.: microRNA-29a-3p Impact on the Neural Stem Cell DifferentiationTo explore how microRNA-29a-3p influences the differentiation of neural stem cells into neurons and to identify any potential mechanisms involved. The program TargetScan, available online was utilized to examine and make predictions about the microRNA-29a-3p located upstream that regulate doublecortin X messenger ribonucleic acid. Ultimately, microRNA-29a-3p was preferred as the main central point of the investigation. The targeting of doublecortin X gene by microRNA-29a-3p was validated by employing a dual-luciferase reporter gene system. Before subjecting to adherent differentiation, the neural stem cells were transfected with microRNA-29a-3p inhibitor, microRNA-29a-3p mimic and normal control. MicroRNA and doublecortin X messenger ribonucleic acid levels were measured through quantitative reverse transcriptionpolymerase chain reaction and doublecortin X protein levels were determined through Western blot assays. The differentiation of neuronal precursor cells was detected by doublecortin X immunofluorescence. Neuronal differentiation was detected by microtubule-associated protein 2 immunofluorescence. According to the dual-luciferase reporter gene system, miR-29a-3p targeted the doublecortin X gene; microRNA-29a-3p significantly decreased in differentiated cells for 3 d was observed, along with a significant reduction in levels of doublecortin X protein and messenger ribonucleic acid. On the other hand, a significant raise in microRNA-29a-3p in differentiated cells of microRNA-29a-3p mimic group for a period of 3 d was noticed with a significant drop in protein levels, doublecortin X messenger ribonucleic acid and doublecortin X immunofluorescence-positive neuronal precursor cells. From the microtubule-associated protein 2 immunofluorescence, it was confirmed that microRNA-29a-3p inhibitor group significantly elevated the total number of neurons, while microRNA-29a-3p mimic reduced the neurons on 7 d. Therefore, low expression of microRNA-29a-3p promote differentiation of neural stem cells into neurons via targeting doublecortin X.

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“…miRNAs are one of these regulatory factors. Currently, there are increasing reports on the study of miRNAs regulating the biological characteristics of NSCs [35][36][37][38] .…”

Section: Resultsmentioning

confidence: 99%

The Impact of microRNA-29a-3p on the Neural Stem Cell Differentiation Process into Neurons

Shi,

Zhou,

Dai

et al. 2023

IJPS

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“…Sepsis-induced neuroin ammation is considered to be a major trigger for hippocampal neurogenesis de cits [39]. A recent study shows that LPS triggers in ammatory cytokines production of astrocytes cultured in vitro, and conditioned medium from LPS-incubated astrocytes can reduce NSCs proliferation and enhance its differentiation into astrocytes [40]. Here, we found that conditioned medium from LPS-stimulated astrocytes impaired the neurogenesis of cultured NSCs; sepsis induced astrocyte-related in ammatory cytokines release and hippocampal neurogenesis de cits in mice.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine attenuates neuroinflammation-mediated hippocampal neurogenesis impairment in sepsis-associated encephalopathy mice through central α2A-adrenoceptor

Guo,

Zhang,

Dai

et al. 2023

Preprint

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Sepsis-associated encephalopathy (SAE), one of the common complications of sepsis, is associated with higher ICU mortality, prolonged hospitalization and long-term cognitive decline. Sepsis can induce neuroinflammation, which negatively affects hippocampal neurogenesis. Dexmedetomidine has been shown to protect against SAE. However, the potential mechanism remains unclear. In this study, we added lipopolysaccharide (LPS)-stimulated astrocytes-conditioned media (LPS-CM) to neural stem cells (NSCs) culture, which were pretreated with dexmedetomidine in the presence or absence of the α2-adrenoceptor antagonist yohimbine or the α2A-adrenoceptor antagonist BRL-44408. LPS-CM impaired the neurogenesis of NSCs, characterized by decreased proliferation, enhanced gliogenesis and declined viability. Dexmedetomidine alleviated LPS-CM-induced impairments of neurogenesis in a dose-dependent manner. Yohimbine, as well as BRL-44408, reversed the effects of dexmedetomidine. We established a mouse model of SAE by cecal ligation and perforation (CLP). CLP induced astrocyte-related neuroinflammation and hippocampal neurogenesis deficits, companied with learning and memory decline, which was reversed by dexmedetomidine. The effect of dexmedetomidine was blocked by BRL-44408. Collectively, our findings support the conclusion that dexmedetomidine can protect against SAE, likely mediated by the combination of inhibiting neuroinflammation via astrocytic α2A-adrenoceptor with attenuating neuroinflammation-induced hippocampal neurogenesis deficits via NSCs α2A-adrenoceptor.

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“…For example, astrocytes stimulated with lipopolysaccharide released bone morphogenetic protein 2 (BMP2), that promoted the differentiation of neural stem cells (NSCs) into astrocytes and inhibited axon remyelination in SCI lesions, and also released EVs enriched with miRNA-22-3p from NSCs [136].…”

Section: Astrocyte-derived Evsmentioning

confidence: 99%

Extracellular Vesicles in the Central Nervous System: A Novel Mechanism of Neuronal Cell Communication

Filannino,

Panaro,

Benameur

et al. 2024

IJMS

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Cell-to-cell communication is essential for the appropriate development and maintenance of homeostatic conditions in the central nervous system. Extracellular vesicles have recently come to the forefront of neuroscience as novel vehicles for the transfer of complex signals between neuronal cells. Extracellular vesicles are membrane-bound carriers packed with proteins, metabolites, and nucleic acids (including DNA, mRNA, and microRNAs) that contain the elements present in the cell they originate from. Since their discovery, extracellular vesicles have been studied extensively and have opened up new understanding of cell–cell communication; they may cross the blood–brain barrier in a bidirectional way from the bloodstream to the brain parenchyma and vice versa, and play a key role in brain–periphery communication in physiology as well as pathology. Neurons and glial cells in the central nervous system release extracellular vesicles to the interstitial fluid of the brain and spinal cord parenchyma. Extracellular vesicles contain proteins, nucleic acids, lipids, carbohydrates, and primary and secondary metabolites. that can be taken up by and modulate the behaviour of neighbouring recipient cells. The functions of extracellular vesicles have been extensively studied in the context of neurodegenerative diseases. The purpose of this review is to analyse the role extracellular vesicles extracellular vesicles in central nervous system cell communication, with particular emphasis on the contribution of extracellular vesicles from different central nervous system cell types in maintaining or altering central nervous system homeostasis.

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Inflammatory stimulation of astrocytes affects the expression of miRNA-22-3p within NSCs-EVs regulating remyelination by targeting KDM3A

Cited by 10 publications

References 71 publications

The Impact of microRNA-29a-3p on the Neural Stem Cell Differentiation Process into Neurons

The Impact of microRNA-29a-3p on the Neural Stem Cell Differentiation Process into Neurons

Dexmedetomidine attenuates neuroinflammation-mediated hippocampal neurogenesis impairment in sepsis-associated encephalopathy mice through central α2A-adrenoceptor

Extracellular Vesicles in the Central Nervous System: A Novel Mechanism of Neuronal Cell Communication

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