Shaoyun Zhao1, Zhe Gong1, Jing Zhang1, Xiaoge Xu1, Peidong Liu2, Wenjuan Guan3, Lijun Jing3, Tao Peng3, Junfang Teng3, Yanjie Jia4. 1. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China; Department of Clinical Medicine, Zhengzhou University, Zhengzhou, China. 2. Department of Clinical Medicine, Zhengzhou University, Zhengzhou, China. 3. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. 4. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: jiayanjie1971@aliyun.com.
Abstract
BACKGROUND: Few studies have examined the relationship between mircroRNAs and moyamoya disease (MMD). We performed a study of the significance of let-7c expression in the serum of MMD patients. METHODS: The experimental group includes 49 MMD patients, and the control group consists of 30 normal people, 20 cerebral hemorrhage patients, 20 massive cerebral infarction patients, 20 nonmassive cerebral infarction patients, and 20 neurological autoimmune disease patients. Let-7 family levels were determined by polymerase chain reaction. A dual luciferase assay was used to test whether let-7c recognized the 3'UTR of RNF213. RESULTS: The expression level of let-7c in MMD patients is higher than that observed in the control groups (P < .001). The luciferase assay results indicated that hsa-let-7c could diminish luciferase activity from a reporter vector containing the 3'-UTR of RNF213 (P < .05). The suppression of luciferase activity is not found in mutRNF213 (P > .05). CONCLUSIONS: Increased expression of let-7c in MMD patients may contribute to MMD pathogenesis by targeting RNF213. Thus, let-7c may be a potential biomarker for the diagnosis of MMD.
BACKGROUND: Few studies have examined the relationship between mircroRNAs and moyamoya disease (MMD). We performed a study of the significance of let-7c expression in the serum of MMD patients. METHODS: The experimental group includes 49 MMD patients, and the control group consists of 30 normal people, 20 cerebral hemorrhagepatients, 20 massive cerebral infarctionpatients, 20 nonmassive cerebral infarctionpatients, and 20 neurological autoimmune diseasepatients. Let-7 family levels were determined by polymerase chain reaction. A dual luciferase assay was used to test whether let-7c recognized the 3'UTR of RNF213. RESULTS: The expression level of let-7c in MMD patients is higher than that observed in the control groups (P < .001). The luciferase assay results indicated that hsa-let-7c could diminish luciferase activity from a reporter vector containing the 3'-UTR of RNF213 (P < .05). The suppression of luciferase activity is not found in mutRNF213 (P > .05). CONCLUSIONS: Increased expression of let-7c in MMD patients may contribute to MMD pathogenesis by targeting RNF213. Thus, let-7c may be a potential biomarker for the diagnosis of MMD.