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  1. Artikel ; Online: Plastic Events of the Vestibular Nucleus: the Initiation of Central Vestibular Compensation.

    Wu, Junyu / Xu, Xue / Zhang, Shifeng / Li, Minping / Qiu, Yuemin / Lu, Gengxin / Zheng, Zhihui / Huang, Haiwei

    Molecular neurobiology

    2024  

    Abstract: Vestibular compensation is a physiological response of the vestibular organs within the inner ear. This adaptation manifests during consistent exposure to acceleration or deceleration, with the vestibular organs incrementally adjusting to such changes. ... ...

    Abstract Vestibular compensation is a physiological response of the vestibular organs within the inner ear. This adaptation manifests during consistent exposure to acceleration or deceleration, with the vestibular organs incrementally adjusting to such changes. The molecular underpinnings of vestibular compensation remain to be fully elucidated, yet emerging studies implicate associations with neuroplasticity and signal transduction pathways. Throughout the compensation process, the vestibular sensory neurons maintain signal transmission to the central equilibrium system, facilitating adaptability through alterations in synaptic transmission and neuronal excitability. Notable molecular candidates implicated in this process include variations in ion channels and neurotransmitter profiles, as well as neuronal and synaptic plasticity, metabolic processes, and electrophysiological modifications. This study consolidates the current understanding of the molecular events in vestibular compensation, augments the existing research landscape, and evaluates contemporary therapeutic strategies. Furthermore, this review posits potential avenues for future research that could enhance our comprehension of vestibular compensation mechanisms.
    Sprache Englisch
    Erscheinungsdatum 2024-04-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-024-04208-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: FGIN-1-27 Mitigates Radiation-induced Mitochondrial Hyperfunction and Cellular Hyperactivation in Cultured Astrocytes.

    Zhang, Shifeng / Deng, Zhezhi / Qiu, Yuemin / Lu, Gengxin / Wu, Junyu / Huang, Haiwei

    Neuroscience

    2023  Band 535, Seite(n) 23–35

    Abstract: Radiation-induced brain injury (RBI) poses a significant challenge in the context of radiotherapy for intracranial tumors, necessitating a comprehensive understanding of the cellular and molecular mechanisms involved. While prior investigations have ... ...

    Abstract Radiation-induced brain injury (RBI) poses a significant challenge in the context of radiotherapy for intracranial tumors, necessitating a comprehensive understanding of the cellular and molecular mechanisms involved. While prior investigations have underscored the role of astrocyte activation and excessive vascular endothelial growth factor production in microvascular damage associated with RBI, there remains a scarcity of studies examining the impact of radiation on astrocytes, particularly regarding organelles such as mitochondria. Thus, our study aimed to elucidate alterations in astrocyte and mitochondrial functionality following radiation exposure, with a specific focus on evaluating the potential ameliorative effects of translocator protein 18 kDa(TSPO) ligands. In this study, cultured astrocytes were subjected to X-ray irradiation, and their cellular states and mitochondrial functions were examined and compared to control cells. Our findings revealed that radiation-induced astrocytic hyperactivation, transforming them into the neurotoxic A1-type, concomitant with reduced cell proliferation. Additionally, radiation triggered mitochondrial hyperfunction, heightened the mitochondrial membrane potential, and increased oxidative metabolite production. However, following treatment with FGIN-1-27, a TSPO ligand, we observed a restoration of mitochondrial function and a reduction in oxidative metabolite production. Moreover, this intervention mitigated astrocyte hyperactivity, decreased the number of A1-type astrocytes, and restored cell proliferative capacity. In conclusion, our study has unveiled additional manifestations of radiation-induced astrocyte dysfunction and validated that TSPO ligands may serve as a promising therapeutic strategy to mitigate this dysfunction. It has potential clinical implications for the treatment of RBI.
    Mesh-Begriff(e) Astrocytes/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Mitochondria/metabolism ; Indoleacetic Acids/metabolism ; Indoleacetic Acids/pharmacology ; Cells, Cultured ; Carrier Proteins/metabolism
    Chemische Substanzen N,N-di-n-hexyl-2-(4-fluorophenyl)indole-3-acetamide (142720-24-9) ; Vascular Endothelial Growth Factor A ; Indoleacetic Acids ; Carrier Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-10-31
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2023.10.017
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Enhanced VEGF secretion and blood-brain barrier disruption: Radiation-mediated inhibition of astrocyte autophagy via PI3K-AKT pathway activation.

    Zhang, Shifeng / Li, Mingping / Qiu, Yuemin / Wu, Junyu / Xu, Xue / Ma, Qian / Zheng, Zhihui / Lu, Gengxin / Deng, Zhezhi / Huang, Haiwei

    Glia

    2023  Band 72, Heft 3, Seite(n) 568–587

    Abstract: Radiation-induced damage to the blood-brain barrier (BBB) is the recognized pathological basis of radiation-induced brain injury (RBI), a side effect of head and neck cancer treatments. There is currently a lack of therapeutic approaches for RBI due to ... ...

    Abstract Radiation-induced damage to the blood-brain barrier (BBB) is the recognized pathological basis of radiation-induced brain injury (RBI), a side effect of head and neck cancer treatments. There is currently a lack of therapeutic approaches for RBI due to the ambiguity of its underlying mechanisms. Therefore, it is essential to identify these mechanisms in order to prevent RBI or provide early interventions. One crucial factor contributing to BBB disruption is the radiation-induced activation of astrocytes and oversecretion of vascular endothelial growth factor (VEGF). Mechanistically, the PI3K-AKT pathway can inhibit cellular autophagy, leading to pathological cell aggregation. Moreover, it acts as an upstream pathway of VEGF. In this study, we observed the upregulation of the PI3K-AKT pathway in irradiated cultured astrocytes through bioinformatics analysis, we then validated these findings in animal brains and in vitro astrocytes following radiation exposure. Additionally, we also found the inhibition of autophagy and the oversecretion of VEGF in irradiated astrocytes. By inhibiting the PI3K-AKT pathway or promoting cellular autophagy, we observed a significant amelioration of the inhibitory effect on autophagy, leading to reductions in VEGF oversecretion and BBB disruption. In conclusion, our study suggests that radiation can inhibit autophagy and promote VEGF oversecretion by upregulating the PI3K-AKT pathway in astrocytes. Blocking the PI3K pathway can alleviate both of these effects, thereby mitigating damage to the BBB in patients undergoing radiation treatment.
    Mesh-Begriff(e) Animals ; Humans ; Blood-Brain Barrier/pathology ; Astrocytes/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Autophagy
    Chemische Substanzen Vascular Endothelial Growth Factor A ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
    Sprache Englisch
    Erscheinungsdatum 2023-11-27
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.24491
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Performance of common buckwheat (Fagopyrum esculentum M.) in response to row spacing under ridge and furrow cropping systems in a semiarid region of China

    Jiang, Ying / Wang, Xinxin / Zeng, Zhaohai / Han, Jinjing / Schiavon, Michala / Tang, Chao / Lu, Gengxin / Lel, Yutian / Li, Jinzhao / Hu, Yuegao / Bu, Yi

    Archives of agronomy and soil science

    2018  Band 64, Heft 8/14, Seite(n) 1807

    Sprache Englisch
    Dokumenttyp Artikel
    ZDB-ID 1132910-5
    ISSN 0365-0340
    Datenquelle Current Contents Ernährung, Umwelt, Agrar

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    Verfügbar in ZB MED Bonn

    Z 1092: Hefte anzeigen

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