机构：[1]Neuroprotection Research Laboratories, Departments of Radiology and Neurology,Massachusetts General Hospital and Harvard Medical School, Boston[2]Clinical Proteomics Research Center, Department of Neurology,Massachusetts General Hospital and Harvard Medical School, Boston[3]Departments of Critical Care Medicine, Neurology, and Neurosurgery, University of Pittsburgh, PA[4]Department of Neurology, Brigham and Women’s Hospital, Boston, MA[5]Cerebrovascular Research Center, Xuanwu Hospital, Capital Medical University, Beijing, China首都医科大学宣武医院[6]Department of Neurology, Massachusetts General Hospital and Program in Neuroscience, Harvard Medical School, Boston
Background and Purpose-Recent studies suggest that extracellular mitochondria may be involved in the pathophysiology of stroke. In this study, we assessed the functional relevance of endogenous extracellular mitochondria in cerebrospinal fluid (CSF) in rats and humans after subarachnoid hemorrhage (SAH). Methods-A standard rat model of SAH was used, where an intraluminal suture was used to perforate a cerebral artery, thus leading to blood extravasation into subarachnoid space. At 24 and 72 hours after SAH, neurological outcomes were measured, and the standard JC1 (5,5', 6,6'-tetrachloro-1,1', 3,3'-tetraethyl-benzimidazolylcarbocyanineiodide) assay was used to quantify mitochondrial membrane potentials in the CSF. To further support the rat model experiments, CSF samples were obtained from 41 patients with SAH and 27 control subjects. Mitochondrial membrane potentials were measured with the JC1 assay, and correlations with clinical outcomes were assessed at 3 months. Results-In the standard rat model of SAH, extracellular mitochondria was detected in CSF at 24 and 72 hours after injury. JC1 assays demonstrated that mitochondrial membrane potentials in CSF were decreased after SAH compared with sham-operated controls. In human CSF samples, extracellular mitochondria were also detected, and JC1 levels were also reduced after SAH. Furthermore, higher mitochondrial membrane potentials in the CSF were correlated with good clinical recovery at 3 months after SAH onset. Conclusions-This proof-of-concept study suggests that extracellular mitochondria may provide a biomarker-like glimpse into brain integrity and recovery after injury.
基金：
National Institutes of Health, the Rappaport Foundation,
the China National Natural Science Foundation Award for Distinguished Young Scholars.
第一作者机构：[1]Neuroprotection Research Laboratories, Departments of Radiology and Neurology,Massachusetts General Hospital and Harvard Medical School, Boston[3]Departments of Critical Care Medicine, Neurology, and Neurosurgery, University of Pittsburgh, PA[4]Department of Neurology, Brigham and Women’s Hospital, Boston, MA
通讯作者：
通讯机构：[*1]Departments of Radiology and Neurology, Neuroprotection Research Laboratories, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129
推荐引用方式(GB/T 7714)：
Sherry H.-Y. Chou,Jing Lan,Elga Esposito,et al.Extracellular Mitochondria in Cerebrospinal Fluid and Neurological Recovery After Subarachnoid Hemorrhage[J].STROKE.2017,48(8):2231-2237.doi:10.1161/STROKEAHA.117.017758.
APA：
Sherry H.-Y. Chou,Jing Lan,Elga Esposito,MingMing Ning,Leonora Balaj...&Kazuhide Hayakawa.(2017).Extracellular Mitochondria in Cerebrospinal Fluid and Neurological Recovery After Subarachnoid Hemorrhage.STROKE,48,(8)
MLA：
Sherry H.-Y. Chou,et al."Extracellular Mitochondria in Cerebrospinal Fluid and Neurological Recovery After Subarachnoid Hemorrhage".STROKE 48..8(2017):2231-2237
医学