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.

译文

据报道,人类巨细胞病毒 (HCMV) 通过诱导新血管形成与血管疾病有关。我们先前已经报道了microRNA (miR)-217和miR-199a-5p通过抑制HCMV感染的人脐静脉内皮细胞 (huvec) 中的sirtuin 1 (SIRT1) 来增强内皮血管生成。在这里,我们发现miR-138还抑制了SIRT1蛋白的表达并刺激了信号转导子和转录激活子3的磷酸化 (p-STAT3)。此外,发现由SIRT1介导的p-STAT3表达调节可促进HCMV诱导的血管生成。这些发现表明,miR-138可能通过激活SIRT1-mediated p-STAT3途径促进HCMV感染的HUVECs的血管生成,这可能为HCMV诱导的血管生成提供新的见解。

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