دورية أكاديمية
Hippocampal Atrophy Following Subarachnoid Hemorrhage Correlates with Disruption of Astrocyte Morphology and Capillary Coverage by AQP4.
العنوان: | Hippocampal Atrophy Following Subarachnoid Hemorrhage Correlates with Disruption of Astrocyte Morphology and Capillary Coverage by AQP4. |
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المؤلفون: | Anzabi M; Department of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark., Ardalan M; Department of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.; Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov, Denmark., Iversen NK; Department of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark., Rafati AH; Translational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov, Denmark.; Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden., Hansen B; Department of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark., Østergaard L; Department of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark. |
المصدر: | Frontiers in cellular neuroscience [Front Cell Neurosci] 2018 Jan 31; Vol. 12, pp. 19. Date of Electronic Publication: 2018 Jan 31 (Print Publication: 2018). |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101477935 Publication Model: eCollection Cited Medium: Print ISSN: 1662-5102 (Print) Linking ISSN: 16625102 NLM ISO Abbreviation: Front Cell Neurosci Subsets: PubMed not MEDLINE |
أسماء مطبوعة: | Original Publication: Lausanne, Switzerland : Frontiers Research Foundation, 2007- |
مستخلص: | Despite successful management of ruptured intracranial aneurysm following subarachnoid hemorrhage (SAH), delayed cerebral ischemia (DCI) remains the main cause of high mortality and morbidity in patients who survive the initial bleeding. Astrocytes play a key role in neurovascular coupling. Therefore, changes in the neurovascular unit including astrocytes following SAH may contribute to the development of DCI and long-term complications. In this study, we characterized morphological changes in hippocampal astrocytes following experimental SAH, with special emphasis on glia-vascular cross-talk and hippocampal volume changes. Four days after induction of SAH or sham-operation in mice, their hippocampal volumes were determined by magnetic resonance imaging (MRI) and histological/stereological methods. Glial fibrillary acid protein (GFAP) immunostained hippocampal sections were examined by stereological techniques to detect differences in astrocyte morphology, and global spatial sampling method was used to quantify the length density of Aquaporin-4 (AQP4) positive capillaries. Our results indicated that hippocampal volume, as measured both by MRI and by histological approaches, was significantly lower in SAH animals than in the sham-operated group. Accordingly, in this animal model of SAH, hippocampal atrophy existed already at the time of DCI onset in humans. SAH induced retraction of GFAP positive astrocyte processes, accompanied by a significant reduction in the length density of AQP4 positive capillaries as well as narrowing of hippocampal capillaries. Meanwhile, astrocyte volume was higher in SAH mice compared with the sham-operated group. Morphological changes in hippocampal astrocytes seemingly disrupt glia-vascular interactions early after SAH and may contribute to hippocampal atrophy. We speculate that astrocytes and astrocyte-capillary interactions may provide targets for the development of therapies to improve the prognosis of SAH. |
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فهرسة مساهمة: | Keywords: MRI; aquaporin-4; astrocyte; hippocampus; subarachnoid hemorrhage |
تواريخ الأحداث: | Date Created: 20180216 Latest Revision: 20220408 |
رمز التحديث: | 20240628 |
مُعرف محوري في PubMed: | PMC5797792 |
DOI: | 10.3389/fncel.2018.00019 |
PMID: | 29445328 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1662-5102 |
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DOI: | 10.3389/fncel.2018.00019 |