SIRT7 Regulates the Vascular Smooth Muscle Cells Proliferation and Migration via Wnt/ β -Catenin Signaling Pathway

Shan

et al. 2019

Preprint

Background: Atherosclerosis (AS) is a multifactorial chronic disease, and vascular smooth muscle cells (VSMCs) plays an important role in the pathology of AS. MicroRNAs regulate multiple cellular biological processes. This study aimed to investigate the clinical value of miR-183-5p in AS patients, and further explored the effects of miR-183-5p on the proliferation and migration of VSMCs.Methods: qRT-PCR was used to test the level of miR-183-5p. The diagnostic value of miR-183-5p for AS patients was assessed by a receiver operating characteristic (ROC) analysis. Cell proliferation and migration were determined via CCK-8 and Transwell assay.Results: MiR-183-5p was highly expressed in AS patients compared with the healthy group. Serum miR-183-5p expression was positively associated with CIMT and CRP in AS patients. The ROC analysis suggested that miR-183-5p had quality to be used as a biomarker with high specificity and sensitivity for AS detection. Overexpression of miR-183-5p promoted the proliferation and migration of VSMCs.Conclusion: MiR-183-5p is highly expressed in AS patients, and overexpression of miR-183-5p promots the cell proliferation and migration of VSMCs. MiR-183-5p may be a key molecular for the diagnosis and treatment of AS in the future.

Section: Discussionmentioning

confidence: 99%

“…It is well recognized that vascular smooth muscle cells (VSMCs) play an important role in the pathological progress of AS [4]. The aberrant behaviors of VSMCs participate in the pathobiology of AS, and are related to other cellular processes such as inflammation, apoptosis and matrix alterations [5].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-183-5p acts as a potential diagnostic biomarker for atherosclerosis and regulates the growth of vascular smooth muscle cell

Shan

et al. 2019

Preprint

“…During the past few decades, they mainly focused on developing algorithms such as level set, watershed, statistical shape model, region growing, active contour model, threshold processing, graph cuts and traditional machine learning methods that require manually extract tumor features. For example, Zhou et al [1] proposed a unified level set method (LSM) for liver tumor segmentation. They used local pixel intensity clustering combined with hidden Markov random field to construct a unified LSM.…”

Section: Introductionmentioning

confidence: 99%

Liver tumor segmentation in CT volumes using an adversarial densely connected network

et al. 2019

BackgroundMalignant liver tumor is one of the main causes of human death. In order to help physician better diagnose and make personalized treatment schemes, in clinical practice, it is often necessary to segment and visualize the liver tumor from abdominal computed tomography images. Due to the large number of slices in computed tomography sequence, developing an automatic and reliable segmentation method is very favored by physicians. However, because of the noise existed in the scan sequence and the similar pixel intensity of liver tumors with their surrounding tissues, besides, the size, position and shape of tumors also vary from one patient to another, automatic liver tumor segmentation is still a difficult task.ResultsWe perform the proposed algorithm to the Liver Tumor Segmentation Challenge dataset and evaluate the segmentation results. Experimental results reveal that the proposed method achieved an average Dice score of 68.4% for tumor segmentation by using the designed network, and ASD, MSD, VOE and RVD improved from 27.8 to 21, 147 to 124, 0.52 to 0.46 and 0.69 to 0.73, respectively after performing adversarial training strategy, which proved the effectiveness of the proposed method.ConclusionsThe testing results show that the proposed method achieves improved performance, which corroborated the adversarial training based strategy can achieve more accurate and robustness results on liver tumor segmentation task.

“…Moreover, abnormal activation or inhibition of the Wnt/β-catenin pathway has been associated with the occurrence of various diseases, including cancers and Parkinson’s disease [11]. In recent years, an increasing number of reports have shown that this pathway is associated with EC dysfunction and AS [13,14]. For example, Wnt-5a protein expression was significantly up-regulated during AS development and was positively correlated with AS severity in animal experiments and human endarterectomy samples [15,16].…”

Section: Introductionmentioning

confidence: 99%

Simvastatin Attenuates H2O2-Induced Endothelial Cell Dysfunction by Reducing Endoplasmic Reticulum Stress

Liu

et al. 2019

Molecules

Atherosclerosis is the pathological basis of cardiovascular disease, whilst endothelial dysfunction (ED) plays a primary role in the occurrence and development of atherosclerosis. Simvastatin has been shown to possess significant anti-atherosclerosis activity. In this study, we evaluated the protective effect of simvastatin on endothelial cells under oxidative stress and elucidated its underlying mechanisms. Simvastatin was found to attenuate H2O2-induced human umbilical vein endothelial cells (HUVECs) dysfunction and inhibit the Wnt/β-catenin pathway; however, when this pathway was activated by lithium chloride, endothelial dysfunction was clearly enhanced. Further investigation revealed that simvastatin did not alter the expression or phosphorylation of LRP6, but reduced intracellular cholesterol deposition and inhibited endoplasmic reticulum (ER) stress. Inducing ER stress with tunicamycin activated the Wnt/β-catenin pathway, whereas reducing ER stress with 4-phenylbutyric acid inhibited it. We hypothesize that simvastatin does not affect transmembrane signal transduction in the Wnt/β-catenin pathway, but inhibits ER stress by reducing intracellular cholesterol accumulation, which blocks intracellular signal transduction in the Wnt/β-catenin pathway and ameliorates endothelial dysfunction.