Ebrahimi Vahid, Rastegar-Moghaddam Seyed Hamidreza, Mohammadipour Abbas
Department of Anatomical Sciences, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mol Neurobiol. 2023 Apr;60(4):2062-2069. doi: 10.1007/s12035-022-03197-4. Epub 2023 Jan 4.
Stroke is a leading cause of death and disability worldwide. It is among the most common neurological disorders with an 8-10% lifetime risk. Ischemic stroke accounts for about 85% of all strokes and damages the brain tissue via various damaging mechanisms. Following cerebral ischemia, the disrupted blood-brain barrier (BBB) leads to cerebral edema formation caused by activation of oxidative stress, inflammation, and apoptosis, targeting primarily endothelial cells. Activation of the protective mechanisms might favor fewer damages to the neural tissue. MicroRNA (miR)-126 is an endothelial cell-specific miR involved in angiogenesis. MiR-126 orchestrates endothelial progenitor cell functions under hypoxic conditions and could inhibit ischemia-induced oxidative stress and inflammation. It alleviates the BBB disruption by preventing an augment in matrix metalloproteinase level and halting the decrease in the junctional proteins, including zonula occludens-1 (ZO-1), claudin-5, and occludin levels. Moreover, miR-126 enhances post-stroke angiogenesis and neurogenesis. This work provides a therapeutic perspective for miR-126 as a new approach to treating cerebral ischemia.
中风是全球死亡和残疾的主要原因。它是最常见的神经系统疾病之一,终生风险为8-10%。缺血性中风约占所有中风的85%,并通过各种损伤机制损害脑组织。脑缺血后,受损的血脑屏障(BBB)会导致脑水肿形成,这是由氧化应激、炎症和凋亡的激活引起的,主要针对内皮细胞。激活保护机制可能有利于减少对神经组织的损伤。微小RNA(miR)-126是一种参与血管生成的内皮细胞特异性miR。miR-126在缺氧条件下协调内皮祖细胞功能,并可抑制缺血诱导的氧化应激和炎症。它通过防止基质金属蛋白酶水平升高和阻止包括紧密连接蛋白-1(ZO-1)、闭合蛋白-5和咬合蛋白水平在内的连接蛋白减少,减轻血脑屏障破坏。此外,miR-126可增强中风后的血管生成和神经发生。这项工作为miR-126作为治疗脑缺血的新方法提供了治疗前景。