scholarly journals Anti-Atherosclerotic Effect of Gossypetin on Abnormal Vascular Smooth Muscle Cell Proliferation and Migration

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1357
Author(s):  
Hui-Hsuan Lin ◽  
Ming-Chang Hsieh ◽  
Chi-Ping Wang ◽  
Pei-Rong Yu ◽  
Ming-Shih Lee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Phase Distribution ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Underlying Mechanism ◽  
Ros Generation ◽  
And Migration ◽  
Cardiovascular Illness ◽  
Proliferation And Migration

Gossypetin (GTIN), known as 3,5,7,8,3′,4′-hexahydroxyflavone, has been demonstrated to exert anti-atherosclerotic potential against apoptotic injury in oxidized low-density lipoprotein-incubated endothelial cells, and atherosclerotic lesions of cholesterol-fed rabbits. However, the effect and underlying mechanism of GTIN on abnormal vascular smooth muscle cells (VSMCs) proliferation and migration, a major event in the pathogenesis of atherosclerosis, is still unknown. In this study, non-cytotoxic doses of GTIN abolished the VSMCs A7r5 proliferation and cell-cycle S phase distribution. The GTIN-arrested G0/G1 phase might be performed by increasing the expressions of phosphorylated p53 and its downstream molecules that inhibit the activation of cyclin E/cyclin-dependent kinase (cdk)-2, blocking retinoblastoma protein (Rb) phosphorylation and the subsequent dissociation of Rb/transcription factor E2F1 complex. In addition, the results indicated that GTIN inhibited VSMCs wound-healing and migratory abilities through reducing matrix metalloproteinase (MMP)-9 activity and expression, as well as down-regulating protein kinase B (PKB)/nuclear factor-kappaB (NF-κB) signaling. GTIN also revealed potential in diminishing reactive oxygen species (ROS) generation. These findings suggested the inhibitory effects of GTIN on VSMCs dysfunction could likely lead to the containment of atherosclerosis and other cardiovascular illness.

scholarly journals MiR-128-3p inhibits vascular smooth muscle cell proliferation and migration by repressing FOXO4/MMP9 signaling pathway

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Chuan Qu ◽  
Xin Liu ◽  
Yan Guo ◽  
Yuhong Fo ◽  
Xiuhuan Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Inflammatory Cytokines ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background MicroRNAs (miRNAs) have been identified as important participants in the development of atherosclerosis (AS). The present study explored the role of miR-128-3p in the dysfunction of vascular smooth muscle cells (VSMCs) and the underlying mechanism. Methods Human VSMCs and ApoE knockout (ApoE−/−) C57BL/6J mice were used to establish AS cell and animal models, respectively. Expression levels of miR-128-3p, forkhead box O4 (FOXO4) and matrix metallopeptidase 9 (MMP9) were detected using qRT-PCR and Western blot, respectively. CCK-8, BrdU, and Transwell assays as well as flow cytometry analysis were performed to detect the proliferation, migration and apoptosis of VSMCs. Levels of inflammatory cytokines and lipids in human VSMCs, mice serum and mice VSMCs were also determined. The binding site between miR-128-3p and 3′UTR of FOXO4 was confirmed using luciferase reporter gene assay. Results MiR-128-3p was found to be decreased in AS patient serum, ox-LDL-treated VSMCs, AS mice serum and VSMCs of AS mice. Transfection of miR-128-3p mimics suppressed the proliferation and migration of VSMCs, accompanied by the promoted apoptosis and the decreased levels of inflammatory cytokines. Further experiments confirmed the interaction between miR-128-3p and FOXO4. Augmentation of FOXO4 or MMP9 reversed the effects of miR-128-3p. Besides, miR-128-3p inhibited triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) but increased high-density lipoprotein cholesterol (HDL-C) in the serum of AS mice. Conclusion MiR-128-3p repressed the proliferation and migration of VSMCs through inhibiting the expressions of FOXO4 and MMP9.

scholarly journals VCAM-1-targeted and PPARδ-agonist-loaded nanomicelles enhanced suppressing effects on apoptosis and migration of oxidized low-density lipoprotein-induced vascular smooth muscle cells

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Gang Wei ◽  
Liangang Hao ◽  
Xueli Li ◽  
Wen Xu ◽  
Fuxiang Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
And Migration

Abstract Purpose: Nanomicelles (NMs) have been widely used for various biomedical applications due to its unique physiochemical properties. The present study aims to investigate the effects of vascular cell adhesion molecule-1 (VCAM-1)-targeted and peroxisome proliferator-activated receptor δ (PPARδ) agonist (GW0742)-loaded NMs on apoptosis and migration in oxidized low-density lipoprotein (ox-LDL)-induced human aortic vascular smooth muscle cells (HAVSMCs). Methods: The GW0742-loaded NMs (M-GW) and VCAM-1-targeted NMs loaded with GW0742 (TM-GW) were prepared, and then the morphologies and the size distribution of M-GM and TM-GM were observed by transmission electron microscopy (TEM) and dynamic light scattering (DLS), respectively. In vitro drug release assay of M-GM and TM-GM were performed as well. Next, HAVSMCs were cultured in medium containing ox-LDL to mimic atherosclerotic environment, and the effects of free GW0742, M-GM and TM-GM on endocytosis, cell migration and apoptosis, as well as the expression of VCAM-1, and proteins associated with migration and apoptosis were measured in HAVSMCs treated with ox-LDL. Results: M-GM and TM-GM were successfully prepared. VCAM-1 was overexpressed in HAVSMCs treated with ox-LDL, and TM-GM had a strong targeting ability to HAVSMCs treated with ox-LDL compared with M-GM. In addition, compared with free GW0742, both M-GM and TM-GM significantly diminished cell apoptosis and migration in HAVSMCs treated with ox-LDL. Conclusions: TM-GM had a superior suppressing effect on apoptosis and migration of ox-LDL-induced HAVSMCs.

Abnormal expression of homeobox c6 in the atherosclerotic aorta and its effect on proliferation and migration of rat vascular smooth muscle cells

2020 ◽  
Vol 52 (9) ◽  
pp. 935-943
Author(s):  
Xiangshu Long ◽  
Ganhua You ◽  
Qiang Wu ◽  
Yu Zhou ◽  
Fuxun Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
P53 Protein ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
And Migration ◽  
Proliferation And Migration

Abstract Homeobox c6 (Hoxc6) affects the proliferation, migration, and infiltration of malignant tumor cells; however, the effect of Hoxc6 on atherosclerosis (AS) as well as the proliferation and migration of vascular smooth muscle cells (VSMCs), which play a role in promoting AS, has not yet been well clarified. In the present study, we tested the hypothesis that Hoxc6 affects the proliferation and migration of rat VSMCs, and hence is involved in AS. The results showed that the expression of Hoxc6 mRNA and protein was higher in normal rat aortic wall than in the myocardium. Subsequently, a rat model of AS was established by high-fat feeding for 2 months. The expression of Hoxc6 mRNA and protein was increased significantly in AS lesions, while the expression of p53 protein was decreased and that of proliferating cell nuclear antigen (PCNA) was increased. Moreover, not only the proliferation and mobility of cells in normal culture were decreased, but also the proliferation was stimulated by oxidized low-density lipoprotein, which was decreased after downregulation of Hoxc6 expression in VSMCs in rat. Consecutively, the expression of PCNA protein was decreased, while that of p53 was increased. These results indicated that Hoxc6 is probably involved in AS via p53 and PCNA by affecting the proliferation and migration of VSMCs.

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