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Downregulation of serum brain specific microRNA is associated with inflammation and infarct volume in acute ischemic stroke

Abstract Cerebral ischemic injury activates a robust inflammatory response, exacerbating neurological deficit. Several brain specific microRNA (miRNA) molecules have been reported to mediate functioning of the immune system, referred to as NeurimmiR. We aimed to explore possible associations between...

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Published in:Journal of clinical neuroscience 2015-02, Vol.22 (2), p.291-295
Main Authors: Liu, Yanping, Zhang, Junjian, Han, Rongfei, Liu, Hanxing, Sun, Dong, Liu, Xuan
Format: Article
Language:English
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Summary:Abstract Cerebral ischemic injury activates a robust inflammatory response, exacerbating neurological deficit. Several brain specific microRNA (miRNA) molecules have been reported to mediate functioning of the immune system, referred to as NeurimmiR. We aimed to explore possible associations between serum miRNA levels and stroke severity and their involvement in the regulation of inflammatory responses after stroke. Blood samples were obtained from 31 patients with acute ischemic stroke and 11 healthy controls. We evaluated infarct volume using diffusion weighted imaging and neurological deficit using the National Institutes of Health Stroke Scale. Serum levels of three NeurimmiR, miR-124, miR-9 and miR-219 were detected by real-time polymerase chain reaction and serum levels of metalloproteinase-9 (MMP-9), a proinflammation marker in brain injury, were examined by enzyme-linked immunosorbent assay. We found that serum miR-124 was significantly decreased within 24 hours after stroke onset and serum miR-9 was decreased in patients with larger stroke. There were no significant changes in serum miR-219. Both serum miR-124 and miR-9 levels within 24 hours were negatively correlated with infarct volume and plasma high-sensitivity C-reactive protein levels. All three NeurimmiR negatively correlated with MMP-9 levels. Our preliminary findings indicate that serum miR-124, miR-9 and miR-219 are suppressed in acute ischemic stroke thus facilitating neuroinflammation and brain injury.
ISSN:0967-5868
1532-2653
DOI:10.1016/j.jocn.2014.05.042