BACKGROUND: The current study aims to investigate the expression and potential role of exosome-derived miR-152-3p in acute ischemic stroke (AIS) patients. METHODS: Exosomes were isolated from AIS patients and healthy controls. The level of exosome miR-152-3p was examined using RT-PCR. Receiver operating characteristic (ROC) curves were used to assess exosome miR-152-3p as a biomarker, and the area under the curve (AUC) was reported. RESULTS: Our data showed that the expression of serum exosome miR-152-3p in patients with AIS was significantly lower than in healthy controls. In contrast to those with NIHSS score < 7, the level of exosome miR-152-3p was significantly reduced in AIS patients with NIHSS score ≥ 7, indicating that the decrease of exosome miR-152-3p level is significantly related to the severity of endothelial injury. Moreover, the lowest level of exosome miR-152-3p was found in large-artery atherosclerosis (LAA) patients compared to that in small-vessel occlusion (SAA), cardioembolism (CE) and stroke of undetermined etiology (SUE) group. In addition, exosome miR-152-3p level was significantly lower in acute phase than in chronic phase. ROC curve showed that the AUC of exosome miR-152-3p level was 0.935, which indicated that exosome miR-152-3p level could distinguish AIS patients from non-healthy controls. CONCLUSIONS: In summary, exosome miR-152-3p is a risk factor of cerebral infarction. Enhancing the expression of exosome miR-152-3p in the circulating system may be a promising strategy for the prevention and treatment of AIS.
BACKGROUND: The current study aims to investigate the expression and potential role of exosome-derived miR-152-3p in acute ischemic stroke (AIS) patients. METHODS: Exosomes were isolated from AIS patients and healthy controls. The level of exosome miR-152-3p was examined using RT-PCR. Receiver operating characteristic (ROC) curves were used to assess exosome miR-152-3p as a biomarker, and the area under the curve (AUC) was reported. RESULTS: Our data showed that the expression of serum exosome miR-152-3p in patients with AIS was significantly lower than in healthy controls. In contrast to those with NIHSS score < 7, the level of exosome miR-152-3p was significantly reduced in AIS patients with NIHSS score ≥ 7, indicating that the decrease of exosome miR-152-3p level is significantly related to the severity of endothelial injury. Moreover, the lowest level of exosome miR-152-3p was found in large-artery atherosclerosis (LAA) patients compared to that in small-vessel occlusion (SAA), cardioembolism (CE) and stroke of undetermined etiology (SUE) group. In addition, exosome miR-152-3p level was significantly lower in acute phase than in chronic phase. ROC curve showed that the AUC of exosome miR-152-3p level was 0.935, which indicated that exosome miR-152-3p level could distinguish AIS patients from non-healthy controls. CONCLUSIONS: In summary, exosome miR-152-3p is a risk factor of cerebral infarction. Enhancing the expression of exosome miR-152-3p in the circulating system may be a promising strategy for the prevention and treatment of AIS.