scholarly journals Cytoglobin overexpression facilitates proliferation and migration of vascular smooth muscle cells

2020 ◽  
Vol 72 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Lei Li ◽  
Yilin Xie ◽  
Shen Li ◽  
Juanjuan Tan ◽  
Yingchun Qin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Feedback Regulation ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
Matrix Remodeling ◽  
Negative Feedback Regulation ◽  
Vsmc Proliferation

Cytoglobin, a recently discovered globin, is expressed in vascular smooth muscle cells (VSMCs). Loss of cytoglobin provides a protective effect on vascular reconstruction but the effect of its overexpression is unclear. The aim of the study was to investigate the effect of cytoglobin overexpression on the migration and proliferation of VSMCs and possible mechanisms. We detected the expression of cytoglobin in hypertensive and normotensive rat aortas, with negative feedback regulation between cytoglobin and hypertension observed. The expression of cytoglobin was significantly decreased in hypertensive rats compared to normotensive rats, but VSMCs overexpressing cytoglobin displayed increased cell migration and proliferation, which led to a phenotypic switch. The increased expression of matrix metalloproteinase 9 and collagen Ia suggests a role for cytoglobin in extracellular matrix remodeling. Increased expression of proliferating cell nuclear antigen and decreased expression of p27 implies that cytoglobin is involved in modulating VSMC proliferation. Our findings indicate that cytoglobin may play an important role in vascular wall remodeling.

Radiation suppresses neointimal hyperplasia through affecting proliferation and apoptosis of vascular smooth muscle cells

2018 ◽  
Vol 19 (2) ◽  
pp. 153-161 ◽  
Author(s):  
Liqin Yuan ◽  
Chang Shu ◽  
Xiao Zhou ◽  
Jiehua Li ◽  
Lunchang Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Neointimal Hyperplasia ◽  
Muscle Cells ◽  
S Phase ◽  
Nuclear Antigen ◽  
X Ray ◽  
Vsmc Proliferation

Purpose: To study the effect of x-ray radiotherapy on vascular smooth muscle cells (VSMCs) and elucidate the mechanisms in preventing neointimal hyperplasia of prosthetic vascular grafts. Materials and methods: In model I, twelve mongrel dogs underwent revascularization with prosthetic grafts and half the dogs underwent irradiation of the grafts at 28 Gy. In model II, human VSMCs (hVSMCs) were maintained and divided into six groups to which external radiation was applied at six different doses: 0 Gy, 2 Gy, 8 Gy, 16 Gy, 24 Gy and 30 Gy. In both models, specimens were harvested and examined by using morphological, immunological, cellular and molecular methods. Results: After irradiation, the neointima thickness was significantly lower in irradiated groups (p≤0.01). The radiotherapy could up-regulate p27kip1, and down-regulate proliferating cell nuclear antigen (PCNA) and S phase kinase associated protein 2 (Skp2). X-ray irradiation inhibits the proliferation of hVSMCs via acting on G1/S phase of cell cycle. The apoptosis of hVSMCs increased significantly with dose and time. The expression of PCNA and Skp2 were decreased after a first increasing trend with dose, but had a significant negative correlation with time. The expression of p27kip1 had a significant positive correlation with dose and time. Conclusions: Postoperative external fractionated irradiation after prosthetic vessel replacement of the abdominal aorta suppressed the development of hyperplasia in the graft neointima in the short term. There was a prominent time- and dose-dependent inhibition of VSMC proliferation by radiation when it was administered.

Abstract 173: MicroRNA-365 Inhibits the Proliferation of Vascular Smooth Muscle Cells by Targeting Cyclin D1

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Myung-Hyun Kim ◽  
Onju Ham ◽  
Se-Yeon Lee ◽  
Eunmi Choi ◽  
Chang Yeon Lee ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cyclin D1 ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
Neointimal Formation ◽  
Vsmc Proliferation

Background: Abnormal proliferation of vascular smooth muscle cells (VSMCs) is a common feature of disease progression in atherosclerosis. Cell proliferation is regulated by cell cycle regulatory proteins. MicroRNAs (miRNAs) have been reported to act as important gene regulators and play essential roles in the proliferation and migration of VSMCs in cardiovascular disease. However, the roles and mechanisms of miRNAs in VSMCs and neointimal formation are far from being fully understood. Methods & Results: In this study, cell cycle specific cyclin D1 was found to be a potential target of miR-365 by direct binding. Through an in vitro experiment, we showed that exogenous miR-365 overexpression reduced VSMC proliferation and proliferating cell nuclear antigen (PCNA) expression, while miR-365 was observed to block G1/S transition in platelet-derived growth factor (PDGF)-induced VSMCs. In addition, the proliferation of VSMCs by various stimuli, including PDGF, angiotensin II (Ang II), and serum, led to the downregulation of miR-365 expression levels. The expression of miR-365 was confirmed in balloon injured carotid arteries. Taken together, our results suggest an anti-proliferative role for miR-365 in VSMC proliferation, at least partly via modulating the expression of cyclin D1. Conclusions: Therefore, miR-365 may influence neointimal formation in atherosclerosis patients.

scholarly journals lncRNA-SNHG14 Promotes Atherosclerosis by Regulating RORα Expression through Sponge miR-19a-3p

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Baoliang Zhu ◽  
Jing Liu ◽  
Ying Zhao ◽  
Jing Yan
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Direct Interaction ◽  
Muscle Cells ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Regulatory Relationship ◽  
Vsmc Proliferation

Coronary heart disease (CHD) is the most common cardiovascular disease with high prevalence, disability, and mortality. The balance between proliferation and apoptosis of vascular smooth muscle cells (VSMCs) plays a key role in the initiation of atherosclerosis. In this study, we found a significant decrease in the expression of lncRNA-SNHG14 in atherosclerotic plaque tissues of ApoE-/- mice. Overexpression of lncRNA-SNHG14 can inhibit VSMC proliferation while promoting apoptosis. There is a potential reciprocal regulatory relationship between lncRNASNHG14 and miR-19a-3p, which inhibit each other’s expression in vascular smooth muscle cells. In addition, the luciferase reporter gene analysis results showed that there was a direct interaction between miR-19a-3p and the 3′UTR of RORα. The results of qRT-PCR showed that the level of RORα mRNA was significantly increased in the aortas treated with miR-19a-3p and SNHG14 compared with that treated with miR-19a-3p alone. In conclusion, we demonstrated that lncRNA-SNHG14 regulates the apoptosis/proliferation balance of VSMCs in atherosclerosis.

Failure of cdc2 promoter activation and G2/M transition by ANG II and AVP in vascular smooth muscle cells

1999 ◽  
Vol 277 (2) ◽  
pp. H515-H523 ◽  
Author(s):  
Nobuya Fujita ◽  
Yusuke Furukawa ◽  
Naoki Itabashi ◽  
Yasushi Tsuboi ◽  
Michio Matsuda ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Physiological Role ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
Ang Ii ◽  
Promoter Activation ◽  
Mrna Induction

The physiological role of the vasoconstrictive hormones arginine vasopressin (AVP) and angiotensin II (ANG II) in the development of vascular hyperplasia is still unclear. We examined the effects of these hormones on cell cycle regulation of cultured rat vascular smooth muscle cells (VSMC). AVP and ANG II were able to induce G1/S transition and DNA synthesis in serum-starved quiescent VSMC but failed to promote further progression into G2/M phases. AVP and ANG II enhanced the expression and activity of cdk2, cyclin E, and proliferating cell nuclear antigen but did not induce expression of cdc2/cyclin B complex, a critical regulator of G2/M transition. The failure of cdc2 mRNA induction was found to be caused by a defect in cdc2 promoter activation. Binding of free E2F-1 to the cdc2 promoter did not occur in hormone-treated VSMC, which may account for the defective induction of cdc2. The absence of cdc2 promoter activation and G2/M transition may be important for the prevention of hyperplasia under physiological conditions but underlies the hypertrophy of VSMC.

Role of the signal transducer and activator of transcription 3 protein in the proliferation of vascular smooth muscle cells

Vascular ◽  
2020 ◽  
Vol 28 (6) ◽  
pp. 821-828
Author(s):  
Hong-Xia Tang ◽  
Xu-Ping Qin ◽  
Jie Li
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Signal Transducer ◽  
Vsmc Proliferation ◽  
Stat3 Signaling Pathway ◽  
Artery Disease ◽  
Transcription 3

Objectives Cardiovascular disease (CVD) remains the primary cause of morbidity and mortality worldwide. The abnormal proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of CVD. The functional and phenotypic changes in vascular cells are mediated by complex signaling cascades that initiate and control genetic reprogramming. Many studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) regulates a diverse array of functions relevant to atherosclerosis. Methods In this review, we summarize the studies on the STAT3-mediated proliferation of VSMCs and subsequent CVDs such as hypertension, atherosclerosis, stroke, coronary artery disease, and myocardial infarction. Furthermore, we describe the general background of STAT3, its structure, function and regulation as well as the STAT3 signaling pathway. Finally, we highlight some potential issues and propose some solutions to these issues. Results and conclusions: STAT3 activation promotes the proliferation of VSMCs by regulating the transcription of genes. Studying the mechanism of VSMC proliferation induced by the STAT3 pathway is valuable for finding therapeutic targets for CVD.

scholarly journals Anti-Proliferative Effect of an Aqueous Extract ofPrunella vulgarisin Vascular Smooth Muscle Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Sun Mi Hwang ◽  
Yun Jung Lee ◽  
Yong Pyo Lee ◽  
Jung Joo Yoon ◽  
So Min Lee ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
P38 Mapk ◽  
Vascular Smooth Muscle Cells ◽  
Aqueous Extract ◽  
High Glucose ◽  
Muscle Cells ◽  
Prunella Vulgaris ◽  
Vsmc Proliferation

The abnormal proliferation of vascular smooth muscle cells (VSMCs) in arterial walls is an important pathogenic factor of vascular disorders such as diabetic atherosclerosis. We have reported the anti-inflammatory effect of an aqueous extract fromPrunella vulgaris(APV) in vascular endothelial cell. In the present study, APV exhibited inhibitory effects on high glucose-stimulated VSMC proliferation, migration, and invasion activities, inducing G1cell cycle arrest with downregulation of cyclins and CDKs and upregulation of the CKIs,p21waf1/cip1andp27kip1. Furthermore, APV dose dependently suppressed the high glucose-induced matrix metalloproteinase activity. High glucose-induced phosphorylation of ERK, p38 MAPK, was decreased by the pretreatment of APV. NF-κB activation by high glucose was attenuated by APV, as an antioxidant. APV attenuated the high glucose-induced decrease of nuclear factor E2-related factor-2 (Nrf2) translocation and heme oxygenase-1 (HO-1) expression. Intracellular cGMP level was also increased by APV treatment. These results demonstrate that APV may inhibit VSMC proliferation via downregulating ROS/NF-κB /ERK/p38 MAPK pathways. In addition, APV has a beneficial effect by the interaction of Nrf2-mediated NO/cGMP with HO-1, suggesting thatPrunella vulgarismay be useful in preventing diabetic atherosclerosis.

scholarly journals Transcriptional Regulation of S Phase Kinase-associated Protein 2 by NR4A Orphan Nuclear Receptor NOR1 in Vascular Smooth Muscle Cells

2011 ◽  
Vol 286 (41) ◽  
pp. 35485-35493 ◽  
Author(s):  
Florence Gizard ◽  
Yue Zhao ◽  
Hannes M. Findeisen ◽  
Hua Qing ◽  
Dianne Cohn ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nuclear Hormone Receptor ◽  
Orphan Nuclear Receptor ◽  
Mobility Shift ◽  
Vsmc Proliferation

Members of the NR4A subgroup of the nuclear hormone receptor superfamily have emerged as key transcriptional regulators of proliferation and inflammation. NOR1 constitutes a ligand-independent transcription factor of this subgroup and induces cell proliferation; however, the transcriptional mechanisms underlying this mitogenic role remain to be defined. Here, we demonstrate that the F-box protein SKP2 (S phase kinase-associated protein 2), the substrate-specific receptor of the ubiquitin ligase responsible for the degradation of p27KIP1 through the proteasome pathway, constitutes a direct transcriptional target for NOR1. Mitogen-induced Skp2 expression is silenced in vascular smooth muscle cells (VSMC) isolated from Nor1-deficient mice or transfected with Nor1 siRNA. Conversely, adenovirus-mediated overexpression of NOR1 induces Skp2 expression in VSMC and decreases protein abundance of its target p27. Transient transfection experiments establish that NOR1 transactivates the Skp2 promoter through a nerve growth factor-induced clone B response element (NBRE). Electrophoretic mobility shift and chromatin immunoprecipitation assays further revealed that NOR1 is recruited to this NBRE site in the Skp2 promoter in response to mitogenic stimulation. In vivo Skp2 expression is increased during the proliferative response underlying neointima formation, and this transcriptional induction depends on the expression of NOR1. Finally, we demonstrate that overexpression of Skp2 rescues the proliferative arrest of Nor1-deficient VSMC. Collectively, these results characterize Skp2 as a novel NOR1-regulated target gene and detail a previously unrecognized transcriptional cascade regulating mitogen-induced VSMC proliferation.

scholarly journals Hexamethylenebisacetamide selectively inhibits the proliferation of human and rat vascular smooth-muscle cells

1992 ◽  
Vol 283 (2) ◽  
pp. 403-408 ◽  
Author(s):  
D J Grainger ◽  
T R Hesketh ◽  
P L Weissberg ◽  
J C Metcalfe
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Maximal Inhibition ◽  
Vsmc Proliferation ◽  
Adp Ribosyltransferase

Hexamethylenebisacetamide (HMBA) selectively and reversibly inhibited proliferation of human and rat vascular smooth-muscle cells (VSMCs) compared with endothelial cells, fibroblasts or lymphocytes. Half-maximal inhibition of VSMC proliferation occurred at 2-5 mM-HMBA, and at 30- greater than 50 mM for other cell types. HMBA also prevented de-differentiation, defined by the loss of smooth-muscle-specific myosin heavy chain, of primary rat VSMCs and caused partial re-differentiation of subcultured cells. Other inhibitors of ADP-ribosyltransferase were also selective inhibitors of VSMC proliferation.

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