miR-138 promotes migration and tube formation of human cytomegalovirus-infected endothelial cells through the SIRT1/p-STAT3 pathway

被引:15
|
作者
Zhang, Shanchao [3 ]
Liu, Lei [2 ]
Wang, Ruijin [1 ]
Tuo, Houzhen [1 ]
Guo, Yanjun [1 ]
Yi, Li [1 ]
Wang, Dexin [1 ]
Wang, Jiawei [2 ]
机构
[1] Capital Med Univ, Beijing Friendship Hosp, Dept Neurol, Beijing 100050, Peoples R China
[2] Capital Med Univ, Beijing Tongren Hosp, Dept Neurol, 1 Dong Jiao Min Xiang, Beijing 100730, Peoples R China
[3] Shandong Univ, Shandong Prov Qianfoshan Hosp, Dept Neurol, Jinan 250014, Shandong, Peoples R China
基金
中国国家自然科学基金; 北京市自然科学基金;
关键词
SMOOTH-MUSCLE-CELLS; DOWN-REGULATION; SIRT1; INFLAMMATION; PROLIFERATION; ANGIOGENESIS; GLIOBLASTOMA; CONTRIBUTES; MECHANISMS; DISEASE;
D O I
10.1007/s00705-017-3423-0
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Human cytomegalovirus (HCMV) has been reported to be linked to vascular disease through the induction of neovessel formation. We have previously reported that microRNA (miR)-217 and miR-199a-5p enhance endothelial angiogenesis via inhibition of sirtuin 1 (SIRT1) in HCMV-infected human umbilical vein endothelial cells (HUVECs). Here, we found that miR-138 also suppressed the expression of the SIRT1 protein and stimulated phosphorylation of signal transducer and activator of transcription 3 (p-STAT3). Moreover, the regulation of p-STAT3 expression mediated by SIRT1 was found to promote HCMV-induced angiogenesis. These findings revealed that miR-138 might promote angiogenesis of HCMV-infected HUVECs by activating the SIRT1-mediated p-STAT3 pathway, and this could provide novel insights into HCMV-induced angiogenesis.
引用
收藏
页码:2695 / 2704
页数:10
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