miR-28-5p improved carotid artery stenosis by regulating vascular smooth muscle cell proliferation and migration.

OBJECTIVES: Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are involved in carotid artery stenosis. The purpose of this study was to investigate the diagnostic value of serum miR-28-5p in asymptomatic carotid artery stenosis and its regulation on the proliferation and migration of VSMCs. METHODS: Serum miR-28-5p levels in 65 healthy controls and 68 asymptomatic carotid artery stenosis patients were detected by qRT-PCR. The receiver-operating characteristic curve was applied to elucidate the diagnostic value of serum miR-28-5p for carotid artery stenosis patients. The specificity of miRNA targets was detected by luciferase reporter assay. CCK-8 and Transwell assay were applied to detect proliferation and migration of cells. Pearson correlation test was used to investigate the correlation between Forkhead box subclass O 1 (FOXO1) and serum miR-28-5p. RESULTS: Serum miR-28-5p was significantly reduced in asymptomatic carotid artery stenosis patients. Moreover, miR-28-5p could distinguish asymptomatic carotid artery stenosis patients from healthy controls, with sensitivity and specificity of 86.8% and 81.5%, respectively, indicating its high diagnostic value. The overexpression of miR-28-5p inhibited the proliferation and migration of VSMCs, while inhibition of miR-28-5p resulted in the opposite effect. What is more, FOXO1, a direct target of miR-28-5p, was significantly increased in asymptomatic carotid artery stenosis patients. Inhibition of miR-28-5p in VSMCs reversed the reduction of FOXO1 levels in patients. CONCLUSIONS: miR-28-5p is a valuable diagnostic biomarker for asymptomatic carotid artery stenosis and can affect the proliferation and migration of VSMCs by regulating FOXO1.

MicroRNA-375-3p is implicated in carotid artery stenosis by promoting the cell proliferation and migration of vascular smooth muscle cells.

BACKGROUND: Atherosclerosis is the main cause of carotid artery stenosis (CAS) which mostly occurs in the elderly. In this paper, the expression level of miR-375-3p in asymptomatic CAS patients and its diagnostic value for asymptomatic CAS were investigated, and the effects of miR-375-3p on the cell proliferation and migration of vascular smooth muscle cells (VSMCs) was further explored. METHODS: 98 healthy subjects and 101 asymptomatic CAS patients were participated in this study. qRT-PCR was used to measure the expression level of serum miR-375-3p, and the ROC curve was established to evaluate the predictive value of miR-375-3p for asymptomatic CAS. After transfection with miR-375-3p mimic or inhibitor in vitro, cell proliferation and migration were detected by CCK-8 assay, colony formation assay, and Transwell assay, respectively. The levels of TNF-α, IL-1ß, IL-6 were detected by ELISA. Western blot was used to detect the protein expression of XIAP. Finally, luciferase reporter gene assay was applied to assess the interaction of miR-375-3p with target genes. RESULTS: The expression level of serum miR-375-3p in asymptomatic CAS patients was significantly higher than that in healthy controls, and the AUC value of ROC curve was 0.888. The sensitivity and specificity were 80.2 and 86.7%, respectively, indicating that miR-375-3p had high diagnostic value for asymptomatic CAS. In vitro cell experiments showed that up-regulation of miR-375-3p significantly promoted the proliferation and migration of VSMCs, and also promoted the generation of inflammatory factors and phenotypic transformation of VSMCs. Luciferase reporter gene assay confirmed that XIAP was a target gene of miR-375-3p and was negatively regulated by miR-375-3p. CONCLUSIONS: In this study, miR-375-3p may have a clinical diagnostic value for asymptomatic CAS patients which need further validation. Increased miR-375-3p levels in CAS may be associated with increased proliferation and migration of VSMCs via downregulation of the apoptosis inducing gene XIAP.

Surgically Clipping a Posterolaterally Projecting Posterior Communicating Artery Aneurysm With Anterior Petroclinoid Fold Fenestration.

The anterior petroclinoid fold (APF) is a ligamentous structure consisting of collagen fiber and extends from the petrous apex to the anterior clinoid process. During the surgical clipping of some posterolaterally projecting posterior communicating artery aneurysms, it may pose a technical challenge due to obscuration of the aneurismal neck by the APF. Herein, the authors describe a simple and effective technique utilizing fenestration of the APF to facilitate visualization and surgical clipping of these aneurysms. To the best knowledge of us, this technique of the APF fenestration has been reported in only a few patients.

microRNA-451 inhibited cell proliferation, migration and invasion through regulation of MIF in renal cell carcinoma.

The expression and functions of microRNA-451 have been studied in many human cancers. However, up to date, there is no study of microRNA-451 in renal cell carcinoma. In the present study, we aimed to investigate the expression, biological functions and molecular mechanisms of microRNA-451 in renal cell carcinoma. microRNA-451 expression level in renal cell carcinoma tissues and cell lines was measured using quantitative Real-time PCR. By using CCK8 assay, cell migration and invasion assay, we explored the functions of microRNA-451 in renal cell carcinoma. Dual-Luciferase report assay, quantitative Real-time PCR and western blot were performed to explore the molecular mechanisms of microRNA-451 functions in renal cell carcinoma. Functional assays were also performed to explore the effects of endogenous MIF in renal cell carcinoma. In this study, we showed for the first time that microRNA-451 was significantly down-regulated in renal cell carcinomas tissues and cell lines. microRNA-451 expression level was correlated with histological grade and lymph node metastasis. In addition, microRNA-451 inhibited proliferation, migration and invasion of renal cell carcinomas cells. Moreover, MIF was identified as a target of microRNA-451, and down-regulation of MIF could mimic the suppressive functions of microRNA-451 in renal cell carcinomas, suggesting that microRNA-451 might be a novel therapeutic strategy for the treatment of renal cell carcinomas.