Annexin A5 derived from lung alleviates brain damage after ischemic stroke

IF 2.7 4区 医学 Q3 NEUROSCIENCES Brain Research Pub Date : 2024-10-29 DOI:10.1016/j.brainres.2024.149303
Jiaxin Hu , Jiaqi Guo , Chuanjie Wu , Xiaoduo He , Jian Jing , Meimei Tao
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Abstract

Ischemic stroke is a leading cause of disability and death worldwide. It is now accepted that brain interacts bidirectionally with other organs after brain diseases. However, factors that might mediate crosstalk between brain and other organs are still less reported. Here we reported that plasma level of Annexin A5, not Annexin A1 or A2, was upregulated in stroke patients when compared to controls. In normal mice, the highest level of Annexin A5 were detected in lung tissues compared with other major organs and lowest level in brain. Moreover, Annexin A5 was increased in brain and decreased in lung after stroke in mice when compared to sham group. Fluorescence in situ hybridization (FISH) assay indicated that Annexin A5 could penetrate the blood–brain barrier (BBB). Treatment with Annexin A5 recombinant protein reduced the infarct volumes and improved neurological function after stroke in mice, while administration of anti-Annexin A5 increased the infarct sizes and aggravated neurological function. In a proof-of-concept analysis, patients with both ischemic stroke and lung diseases had a lower plasma Annexin A5 level than those with only ischemic stroke. Furthermore, Annexin A5 level in bronchoalveolar lavage fluid (BALF) was lower in patients with severe chronic obstructive pulmonary disease (COPD) when compared with those at a less severe grade of COPD, and level of Annexin A5 was positively correlated with forced expiratory volume in 1 s/prediction (FEV1pred) and PaO2. Our results suggest that Annexin A5 could alleviate infarct area and improve general neurological performance post cerebral ischemia. Increased Annexin A5 may derive from lung tissue and permeate across BBB to provide a neuroprotective function. Therefore, Annexin A5 may potentially serve as a therapeutic candidate for defending against IS-induced brain injury.
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源自肺部的附录蛋白 A5 可减轻缺血性中风后的脑损伤。
缺血性中风是全球致残和致死的主要原因。脑部疾病发生后,大脑与其他器官之间的双向互动已被公认。然而,可能介导脑与其他器官之间相互影响的因素仍鲜有报道。在此,我们报告了与对照组相比,脑卒中患者血浆中的附件蛋白 A5(而非附件蛋白 A1 或 A2)水平上调。在正常小鼠中,与其他主要器官相比,肺组织中的附件蛋白 A5 水平最高,而脑中的水平最低。此外,与假组相比,脑卒中后小鼠脑中的 Annexin A5 增加,肺中的 Annexin A5 减少。荧光原位杂交(FISH)检测表明,Annexin A5可穿透血脑屏障(BBB)。用Annexin A5重组蛋白治疗可缩小小鼠中风后的梗死体积并改善神经功能,而服用抗Annexin A5则会扩大梗死体积并加重神经功能。在概念验证分析中,缺血性中风和肺部疾病患者的血浆附件蛋白 A5 水平低于仅患有缺血性中风的患者。此外,严重慢性阻塞性肺病(COPD)患者支气管肺泡灌洗液(BALF)中的 Annexin A5 含量低于病情较轻的慢性阻塞性肺病患者,且 Annexin A5 含量与 1 秒用力呼气容积(FEV1)和 PaO2 呈正相关。我们的研究结果表明,Annexin A5可减轻脑缺血后的梗死面积并改善一般神经功能表现。增加的Annexin A5可能来自肺组织并通过BBB渗透,从而提供神经保护功能。因此,Annexin A5 有可能成为抵御 IS 引起的脑损伤的候选疗法。
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来源期刊
Brain Research
Brain Research 医学-神经科学
CiteScore
5.90
自引率
3.40%
发文量
268
审稿时长
47 days
期刊介绍: An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.
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