Abstract
BackgroundThe relationship between circulating microRNA-223 and pathogenesis of acute ischemic stroke is unknown. Here we investigated the roles and possible targets of circulating microRNA-223 in human ischemic stroke within the first 72 hours.MethodsBlood samples were collected from patients within 72 hours after cerebral ischemia (n = 79) and compared with healthy control samples (n = 75). The level of possible downstream factors of microRNA-223 including insulin-like growth factor-1, insulin-like growth factor-1 receptor and interleukin-6 was examined by ELISA assay. The relationship between the microRNA-223 level and NIHSS scores, TOAST subtypes, and infarct volume was analyzed respectively. In addition, twelve adult male CD-1 mice underwent middle cerebral artery occlusion using the suture technique. Circulating blood and brain tissue in the ischemic ipsilateral hemisphere were collected at 24 hours after middle cerebral artery occlusion. microRNA-223 was detected by real-time polymerase chain reactions.ResultsmicroRNA-223 levels in the circulating blood of acute ischemic stroke patients were greatly increased compared to the control (p < 0.05). microRNA-223, which were negatively correlated with NIHSS scores (r = −0.531, p < 0.01) and infarct volume (r = −0.265, p = 0.039), was significantly up-regulated in large artery and small artery strokes. The plasma level of insulin-like growth factor-1 was positively associated with that of microRNA-223 (r = 0.205, p = 0.022). Moreover, microRNA-223 in blood and brain were positively correlated (r = 0.834, p < 0.05), and they were up-regulated significantly in mice that underwent middle cerebral artery occlusion (p < 0.05).ConclusionsOur results suggest that microRNA-223 is associated with acute ischemic stroke and possibly plays a role in stroke through up-regulating growth factor such as insulin-like growth factor-1 gene.
Highlights
The relationship between circulating microRNA-223 and pathogenesis of acute ischemic stroke is unknown
To explore the regulatory mechanism of miR-223 in the ischemic pathological process, we studied the down-stream insulin-like growth factor1 (IGF-1), insulin-like growth factor-1 receptor (IGF1R) and IL-6 changes in stroke patients
The results of logistic regression suggested that the level of blood miR-223 was a stroke risk factor (p = 0.011, adjusted odd ratio = 1.002, 95% confidence intervals (95% CI): 1.000-1.004)
Summary
The relationship between circulating microRNA-223 and pathogenesis of acute ischemic stroke is unknown. We investigated the roles and possible targets of circulating microRNA-223 in human ischemic stroke within the first 72 hours. MiRNAs are important regulators of the development and function of the brain [2]. Great attention has been paid to miR-223 because it can regulate cell cycle, tumor invasiveness, haematopoietic differentiation and immune cell function [13]. Some known transcriptional factors including NFI-A and C/EBPα regulate miR223 expression [14]. Studies demonstrated that miR-223 is mainly expressed in bone marrow and plays an important role in granulopoiesis [15]. During differentiation or tumor progression, miR-223 suppresses cell proliferation by targeting insulin-like growth factor-1 receptor (IGF1R) [17]. In hepatic ischemia/reperfusion injury, miR-223 is greatly up-regulated and positively correlates with serum markers of ischemic injury [18]. In the central nervous system miR223 is highly present and is neuroprotective by targeting GluR2 and NR2B subunits of the glutamate receptor [19]
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