Myelination defects in the medial prefrontal cortex of
            <i>Fkbp5</i>
            knockout mice

Choi, Kyoung Soon; Lee, Joon‐Hee; Kang, Hyo Jung

doi:10.1096/fj.202001883r

Cited by 12 publications

(6 citation statements)

References 79 publications

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“…Among them, KIF5C is a protein‐coding gene that belongs to Kinesin 1. Over the years, KIF5C has been studied primarily in the nervous system (Choi et al, 2021); it can maintain the function of motor neurons and promote peripheral migration of the ganglion (DuRaine et al, 2018; Kanai et al, 2000). Studies have shown that KIF5C mutations are associated with cerebral cortical malformations and neurodevelopmental disorders, manifested as epileptic seizures in infants, neurobehavioral problems, including speech/language development deficits and a unique spectrum of brain malformations (Michels et al, 2017; Poirier et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Jiang

Chen

et al. 2023

Int Endodontic J

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Aim To investigate the regulatory role of miR‐155 and Kinesin Superfamily Proteins‐5C (KIF‐5C) in the progression of pulpitis based on bioinformatic analysis. Methodology Normal pulp tissues and pulpitis pulp tissues were collected and subjected to high‐throughput sequencing and the differentially expressed miRNAs were determined. An in vitro and in vivo pulpitis model was established. HE, IHC staining and histological evaluation were used to verify the inflammatory state of human and mouse pulp tissues. The mRNA expression of IL‐1β and TGF‐β1 were determined by RT‐qPCR and protein expression of IL‐1α, IL‐4, IL‐8, IL‐13, IFN‐γ, IL‐6, IL‐10 and MCP‐1 were determined by protein chip. The target genes of miR‐155 were predicted by miRanda database and verified by Dual‐luciferase reporter assay, RT‐qPCR and western blotting. MiR‐155 lentivirus were used to upregulate or downregulate miR‐155 and the siRNA of KIF‐5C was used to downregulate KIF‐5C. The expression of miR‐155 or KIF‐5C was determined by RT‐qPCR. All statistics were analysed using GraphPad prism 8.2. Results The high‐throughput sequencing results showed that 6 miRNAs (miR‐155, miR‐21, miR‐142, miR‐223, miR‐486, miR‐675) were significantly upregulated in diseased human pulp tissues, and miR‐155 was significantly elevated among the six miRNAs. RT‐qPCR results demonstrated that miR‐155 expression was upregulated in human pulpitic tissue, mice pulpitic tissue and LPS‐HDPCs. IL‐1β was increased while TGF‐β1 was decreased in lenti‐miR‐155 transfected LPS‐HDPCs. Analysis of protein chip results indicated that lenti‐miR‐155 transfected LPS‐HDPCs produced higher levels of IL‐8, IL‐6, MCP‐1. The opposite results were obtained when miR‐155 was inhibited. Through miRanda database screen and Dual‐luciferase reporter assay, the target gene (KIF‐5C) of miR‐155 was identified. In lenti‐miR‐155 transfected LPS‐HDPCs, the expression of KIF‐5C was downregulated. However, when shRNA‐miR‐155 was transfected to LPS‐HDPCs, the opposite result was obtained. Silent RNA was used to knock down KIF‐5C, the results showed that when both KIF‐5C and miR‐155 were knocked down simultaneously, the downregulated expression of inflammatory factors observed in LPS‐HDPCs following miR‐155 knockdown was rescued. Conclusion MiR‐155 plays an important role in promoting pulpitis through targeting KIF‐5C and may serve as a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Jiang

Chen

et al. 2023

Int Endodontic J

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“…Fkbp5 , encoding for FK506-binding protein 5, was another strongly induced transcript in oligodendrocytes at 7 dpi. It has previously been shown to be induced by glucocorticoids ( Hähle et al, 2019 ) and involved in myelination in the prefrontal cortex ( Choi et al, 2021 ). One of the main functions of oligodendrocytes is myelin formation around neuronal axons and the metabolic support of these to ensure neuronal signalling and information processing ( Lee et al, 2012 ; Moore et al, 2020 ; Saab et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Molecular consequences of peripheral Influenza A infection on cell populations in the murine hypothalamus

Lemcke

Egebjerg

Berendtsen

et al. 2023

eLife

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Infection with Influenza A virus (IAV) causes the well-known symptoms of the flu, including fever, loss of appetite and excessive sleepiness. These responses, mediated by the brain, will normally disappear once the virus is cleared from the system, but a severe respiratory virus infection may cause long-lasting neurological disturbances. These include encephalitis lethargica and narcolepsy. The mechanisms behind such long lasting changes are unknown. The hypothalamus is a central regulator of the homeostatic response during a viral challenge. To gain insight into the neuronal and non-neuronal molecular changes during an IAV infection, we intranasally infected mice with an H1N1 virus and extracted the brain at different time points. Using single-nucleus RNA sequencing (snRNA-seq) of the hypothalamus, we identify transcriptional effects in all identified cell populations. The snRNA-seq data showed the most pronounced transcriptional response at 3 days past infection, with a strong downregulation of genes across all cell types. General immune processes were mainly impacted in microglia, the brain resident immune cells, where we found increased numbers of cells expressing pro-inflammatory gene networks. In addition, we found that most neuronal cell populations downregulated genes contributing to the energy homeostasis in mitochondria and protein translation in the cytosol, indicating potential reduced cellular and neuronal activity. This might be a preventive mechanism in neuronal cells to avoid intracellular viral replication and attack by phagocytosing cells. This is complemented by increased activity of microglia monitoring their surroundings.

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“…Studies suggest that FKBP5 may be a candidate gene for human PTSD treatment. FKBP5 regulates hypothalamic-pituitary-adrenal axis (HPA) activity and regulates stressful stimuli (Choi et al, 2021 ). When subjects encounter threatening cues or stressful triggers, the HPA axis is activated, and the adrenal glands release glucocorticoids (e.g., cortisol in humans or corticosterone in rodents).…”

Section: Neurobiological Mechanisms Of Fear Extinctionmentioning

confidence: 99%

Update on neurobiological mechanisms of fear: illuminating the direction of mechanism exploration and treatment development of trauma and fear-related disorders

Liu

Zhi

et al. 2023

Front. Behav. Neurosci.

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Fear refers to an adaptive response in the face of danger, and the formed fear memory acts as a warning when the individual faces a dangerous situation again, which is of great significance to the survival of humans and animals. Excessive fear response caused by abnormal fear memory can lead to neuropsychiatric disorders. Fear memory has been studied for a long time, which is of a certain guiding effect on the treatment of fear-related disorders. With continuous technological innovations, the study of fear has gradually shifted from the level of brain regions to deeper neural (micro) circuits between brain regions and even within single brain regions, as well as molecular mechanisms. This article briefly outlines the basic knowledge of fear memory and reviews the neurobiological mechanisms of fear extinction and relapse, which aims to provide new insights for future basic research on fear emotions and new ideas for treating trauma and fear-related disorders.

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Myelination defects in the medial prefrontal cortex of Fkbp5 knockout mice

Abstract: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Cited by 12 publications

References 79 publications

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Overexpression of MicroRNA‐155 aggravates pulpitis by targeting kinesin superfamily Proteins‐5C based on illumina high‐throughput sequencing

Molecular consequences of peripheral Influenza A infection on cell populations in the murine hypothalamus

Update on neurobiological mechanisms of fear: illuminating the direction of mechanism exploration and treatment development of trauma and fear-related disorders

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