scholarly journals Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 275
Author(s):  
Chin-Chuan Chen ◽  
Hung-Yuan Li ◽  
Yann-Lii Leu ◽  
Yu-Ju Chen ◽  
Chia-Jen Wang ◽  
...  
Keyword(s):  
Flavonoid Compound ◽  
Ros Production ◽  
Monocyte Adhesion ◽  
Vascular Cell ◽  
Vsmc Proliferation ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
And Migration ◽  
Deficient Mice ◽  
Proliferation And Migration

Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) proliferation and migration, which result in atherosclerotic plaque formation. Corylin, a flavonoid compound, is known to exhibit antioxidative, anti-inflammatory and antiproliferative effects. However, it remains unknown whether corylin could modulate atherogenesis. Here, we identified the anti-inflammatory effect of corylin in tumor necrosis factor-α (TNF-α)-induced vascular cells. In human umbilical vein endothelial cells (HUVECs), corylin suppressed TNF-α-induced monocyte adhesion to the HUVECs and transmigration by downregulating the ROS/JNK/nuclear factor-kappa beta (NF-κB) p65 pathway. In VSMCs, corylin inhibited TNF-α-induced monocyte adhesion by suppressing ROS production, mitogen-activated protein kinase (MAPK) phosphorylation and NF-κB p65 translocation. In platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs, corylin inhibited PDGF-BB-induced VSMC proliferation and migration through regulating the mammalian target of rapamycin (mTOR)/dynamin-1-like protein 1 (Drp1) signaling cascade. In addition, corylin treatment not only attenuated atherosclerotic lesions, ROS production, vascular cell adhesion protein-1 (VCAM-1) expression, monocyte adhesion and VSMC proliferation in apolipoprotein E (ApoE)-deficient mice but also inhibited neointimal hyperplasia in endothelial-denuded mice. Thus, corylin may be a potential prevention and treatment for atherosclerosis.

Extract of Housefly (Musca domestica) Maggot Anti-Inflammatory Parts could Regulate the Proliferation and Migration of TNF-α- Stimulated Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 884-885 ◽  
pp. 446-449
Author(s):  
Fu Jiang Chu ◽  
Hong Yan Ma ◽  
Xiao Bao Jin ◽  
Jia Yong Zhu
Keyword(s):  
Endothelial Cells ◽  
Treatment Group ◽  
Umbilical Vein ◽  
House Fly ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells ◽  
Proliferation And Migration

House fly maggot, Musca domestica (Linnaeus) (Diptera: Muscidae) is one of the traditional Chinese medicine (TCM). In our earlier studies, the anti-inflammatory and anti-atherosclerotic functions of the housefly maggot have been found and also the anti-inflammatory effective parts have been acquired. In this study, the effect of housefly maggot anti-inflammatory parts on proliferation and migration of TNF-α-stimulated human umbilical vein endothelial cells (HUVEC) were investigated. And the results showed that the proliferation index and the migration rates of HUVEC which stimulated by TNF-α were decreased significantly in housefly maggot anti-inflammatory parts treatment group. And also the secretion of vascular endothelial growth factor (VEGF) was decreased too compared with only TNF-α treatment group. Based on the above, the housefly maggot anti-inflammatory parts could regulate the endothelial cell dysfunction through decreasing cell proliferation and migration and a reduction in VEGF expression might plays a key role in this process.

scholarly journals Identification of a Novel Gene Correlated With Vascular Smooth Muscle Cells Proliferation and Migration in Chronic Thromboembolic Pulmonary Hypertension

2021 ◽  
Vol 12 ◽  
Author(s):  
Feng Wang ◽  
Congrui Sun ◽  
Xiaoshuo Lv ◽  
Mingsheng Sun ◽  
Chaozeng Si ◽  
...  
Keyword(s):  
Vascular Remodeling ◽  
Molecular Mechanisms ◽  
Kegg Pathway ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Vsmc Proliferation ◽  
Kegg Pathway Analysis ◽  
Tnf Α ◽  
Thromboembolic Pulmonary Hypertension ◽  
And Migration ◽  
Proliferation And Migration

Objective: Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by thrombofibrotic obstruction of the proximal pulmonary arteries, which result in vascular remodeling of the distal pulmonary artery. While the cellular and molecular mechanisms underlying CTEPH pathogenesis remain incompletely understood, recent evidence implicates vascular remodeling. Here, we identify the molecular mechanisms that contribute to vascular remodeling in CTEPH.Methods: Microarray data (GSE130391) for patients with CTEPH and healthy controls were downloaded from the Gene Expression Omnibus (GEO) and screened for differentially expressed genes (DEGs). DEGs were functionally annotated using Gene Ontology (GO) functional analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. A protein–protein interaction (PPI) network was constructed to identify hub genes. Finally, pulmonary artery samples were harvested from patients with CTEPH (n = 10) and from controls (n = 10) and primary vascular smooth muscle cells (VSMCs) were cultured. Effects of the proto-oncogene FOS on VSMC proliferation and migration were assessed using expression and knockdown studies.Results: We detected a total of 292 DEGs, including 151 upregulated and 141 downregulated genes. GO analysis revealed enrichment of DEGs in biological processes of signal transduction, response to lipopolysaccharide, signal transduction, and myeloid dendritic cell differentiation. Molecular function analysis revealed enrichment in tumor necrosis factor (TNF)-activated receptor activity, transcriptional activator activity, and protein homodimerization activity. The expression of TNF-α and its receptor (sTNFR1 and sTNFR2) were significantly higher in CTEPH group, compared with control group. KEGG pathway analysis revealed enrichment in salmonella infection, pathways in cancer, osteoclast differentiation, and cytokine-cytokine receptor interaction. Hub genes in the PPI included FOS, suggesting an important role for this gene in vascular remodeling in CTEPH. Primary VSMCs derived from patients with CTEPH showed increased FOS expression and high proliferation and migration, which was attenuated by FOS inhibition. In control VSMCs, TNF-α treatment increased proliferation and migration, which FOS inhibition likewise attenuated.Conclusion: TNF-α drives CTEPH pathogenesis by promoting VSMC proliferation and migration via increased FOS expression. These results advance our understanding of the molecular mechanisms of vascular remodeling in CTEPH, and may inform the development of new therapeutic targets.

Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1

2012 ◽  
Vol 50 (9) ◽  
pp. 3025-3031 ◽  
Author(s):  
Siyu Chen ◽  
Yan Ding ◽  
Weiwei Tao ◽  
Wenxiang Zhang ◽  
Tingming Liang ◽  
...  
Keyword(s):  
Vsmc Proliferation ◽  
Tnf Α ◽  
And Migration ◽  
Proliferation And Migration

Sp1, acetylated histone-3 and p300 regulate TRAIL transcription: Mechanisms of PDGF-BB-mediated VSMC proliferation and migration

2012 ◽  
Vol 113 (8) ◽  
pp. 2597-2606 ◽  
Author(s):  
Nor Saadah M. Azahri ◽  
Belinda A. Di Bartolo ◽  
Levon M. Khachigian ◽  
Mary M. Kavurma
Keyword(s):  
Vsmc Proliferation ◽  
Histone 3 ◽  
And Migration ◽  
Proliferation And Migration

Abstract 497: 5-Methoxytryptophan Protects Against Vascular Remodeling

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yen-Chun Ho ◽  
Meng-Ling Wu ◽  
Chen-Hsuan Su ◽  
Cheng-Chin Kuo ◽  
Kenneth K Wu ◽  
...  
Keyword(s):  
Vascular Disease ◽  
P38 Mapk ◽  
Vessel Wall ◽  
Neointima Formation ◽  
Phenotypic Modulation ◽  
Mapk Activation ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Vascular smooth muscle cells (VSMCs) in the blood vessel wall exhibit a differentiated phenotype; their main function is contraction and to regulate vascular tone. In response to injury, VSMCs undergo a phenotypic transition whereby they proliferate and migrate from the medial layer into the intima, contributing to lesion formation and atherosclerosis. 5-methoxytryptophan (5-MTP), a recently identified novel tryptophan metabolite, has been shown to inhibit cancer cell growth, migration, and cancer metastasis. We hypothesized that 5-MTP might play an analogous role in vascular disease as in tumorigenesis. To test our hypothesis, we subjected 12 weeks old C57BL/6 mice to a carotid artery cessation of blood flow model to induce neointima formation. Following surgery, mice were treated with vehicle (PBS) or 100 mg/kg of 5-MTP by intraperitoneal injection 3 times a week. Four weeks later, carotid arteries were harvested for histological analysis. H&E and elastin staining revealed robust neointima in ligated carotids of vehicle-treated mice. In contrast, 5-MTP significantly attenuated neointima formation. Given that proinflammatory cytokine interleukin 1 beta (IL-1β) is increased in the injured vessel wall, we examined whether IL-1β affected VSMC phenotypic modulation. Indeed, IL-1β downregulated VSMC marker SM α-actin expression and increased VSMC proliferation and migration. Importantly, in VSMCs, 5-MTP attenuated IL-1β-mediated SM α-actin downregulation, proliferation, and migration, suggesting a potential role of 5-MTP in controlling VSMC phenotypic modulation. Furthermore, 5-MTP inhibited IL-1β-mediated p38 MAPK activation. Inhibiting p38 MAPK activation by SB203580 dose-dependently decreased IL-1β-induced VSMC proliferation. Taken together, our results suggest an important role of 5-MTP in vascular disease.

Abstract 417: Adenosine Diphosphate Ribosyl Cyclase via PI3K-Akt and FOXO3a Up-regulating MMP-9 to Enhance Vascular Smooth Muscle Cell Proliferation and Migration in Mice

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Yuming Li ◽  
Haitao Li ◽  
Xinfang Wang ◽  
Junya Wang ◽  
Zhongqiu Li
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Adenosine Diphosphate ◽  
High Fat ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

The current study was designed to explore the mechanisms of vascular smooth muscle cell (VSMC) proliferation and migration induced by adenosine diphosphate ribosyl cyclase(ADPRC). In this study, 32 Male ApoE-/- mice(6 weeks old, 18-22g)on a C57BL/6J background were divided into four groups, which received normal chow (n=8, NC group), high-fat Western-type diet (n=8, 0.25% cholesterol, 21% fat,HFD group), high-fat Western-type diet,infusion of 2,2′-dihydroxyazobenzene(DHAB, a ADPRC inhibitor, 2mg/kg/day, n=8, HFD-DHAB group) intraperitoneally or high-fat Western-type diet,infusion of LY294002(a Inhibitor of Akt, 5mg/kg/d, n=8, HFD-LY group) intraperitoneally, for 10 weeks. 8 male C57BL/6J mice served as control. After 10 weeks, mice were anesthetized with chloral hydrate, aorta was removed and immediately frozen in liquid nitrogen. Aortic atherosclerotic lesions, VSMC proliferation and migration were assessed by histomorphological observation, smooth muscle actin-α(α-SMA)and proliferating cell nuclear antigen (PCNA) examination. ADPRC expression and alterations of Akt, FOXO3a, phospho-FOXO3a and MMP-9 were determined by RT-PCR, Western Blot, Immunohistochemistry or Immunofluorescence. The results showed that, in aortic atherosclerotic lesions derived from atherosclerotic mice of HFD group, an increased VSMC proliferation and migration, reflected by the up-regulation of α-SMA and PCNA expression, were observed followed by increased expression of ADPRC, Akt, FOXO3a, phospho-FOXO3a and MMP-9. The enhanced expression of ADPRC and followed alterations of FOXO3a, phospho-FOXO3a, MMP-9 as well as α-SMA, PCNA, VSMC proliferation and migration were absent in NC group and C57BL/6J control mice. Treatment with DHAB or LY294002 reversed VSMC proliferation, migration and expression of Akt, FOXO3a, phospho-FOXO3a and MMP-9 in HFD-DHAB and HFD-LY group. These data shows that high-fat Western-type diet induced ADPRC may via PI3K-Akt to phosphorylate FOXO3a up-regulating MMP-9 to enhance vascular smooth muscle cell proliferation and migration in mice.

Abstract 187: Regulation of Vascular Smooth Muscle Cell (VSMC) Inflammation and Migration by the Pro-resolving Lipid Mediator Maresin-1 (mar1)

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Anuran Chatterjee ◽  
Robert Toy ◽  
Giorgio Mottola ◽  
Mian Chen ◽  
Michael S Conte
Keyword(s):  
Actin Polymerization ◽  
Inflammatory Responses ◽  
Oxidant Stress ◽  
Lipid Mediator ◽  
Monocyte Adhesion ◽  
Inflammatory Gene Expression ◽  
New Class ◽  
Tnf Α ◽  
And Migration ◽  
Inflammatory Molecules

Introduction Resolution of acute inflammation is regulated by endogenous lipid mediators derived from polyunsaturated fatty acids such as docosahexaenoic acid (DHA), however little is known about mechanisms of resolution in vascular injury. We investigated the effects of the DHA-derived mediator Mar1 on VSMC phenotype responses. Methods Primary human VSMCs were obtained from saphenous vein. VSMC were pretreated with Mar1 (10-100nM) then exposed to TNF-α (10ng/ml), and inflammatory responses assessed using a monocyte adhesion (U937) assay, expression of cell adhesion molecules and pro-inflammatory molecules (qPCR, western blot, ELISA), and production of superoxide (DHE). VSMC migration was measured in a transwell assay with PDGF-AB as the agonist, and cyotskeletal changes were assessed by actin-phalloidin staining. Results Mar-1 (100 nM) reduced U937 adhesion to TNF-stimulated VSMC, VCAM-1, and pro-inflammatory cytokine (IL-6, IL-8) expression. Superoxide production measured by DHE fluorescence was reduced by 57% (p=0.002) and Nox4 expression was markedly attenuated (43%, p=0.01). Mar-1 (0.01-100nM) induced rapid cytoskeletal changes with increased cell area, and reduced VSMC migration (76%, p=0.004) to PDGF-AB (50ng/ml; Figure). Conclusions Mar-1 attenuates TNF-α inflammatory activation of VSMC, with reduction in pro-inflammatory gene expression, oxidant stress, and monocyte adhesion. Mar-1 reduces actin polymerization and inhibits VSMC chemotaxis to PDGF. Pro-resolving mediators may represent a new class of endogenous vascular therapeutics.

scholarly journals Methanolic Extract of Distemonanthus benthamianus (Caesalpiniaceae) Stem Bark Suppresses Ethanol/Indomethacin-Induced Chronic Gastric Injury in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Vanessa Mba Matah Marte ◽  
Gilbert Ateufack ◽  
Marius Mbiantcha ◽  
Albert Donatien Atsamo ◽  
Carine Flore Adjouzem ◽  
...  
Keyword(s):  
Methanolic Extract ◽  
Protein Denaturation ◽  
Hematological Parameters ◽  
Mechanisms Of Action ◽  
Male Rats ◽  
Gastric Ulcers ◽  
Gastric Injury ◽  
Ros Production ◽  
Tnf Α ◽  
Anti Inflammatory

Distemonanthus benthamianus (Caesalpiniaceae) is a plant from the Cameroon pharmacopoeia very widely used in the treatment of many pathologies among which are gastrointestinal disorders. The main purpose of this study was to assess the healing properties of gastric ulcer from the methanolic extract of Distemonanthus benthamianus and its mechanisms of action. The healing properties of gastric ulcers (chronic ulcer model induced by ethanol and indomethacin) were evaluated in vivo in adult male rats, while the mechanisms of action were evaluated in vitro by anti-inflammatory assay (protein denaturation, cyclooxygenase, and lipoxygenase assays) and immunomodulatory assay (ROS production (using technical chemiluminescence), cytokine (TNF-α, IL-1β, IL-6) production (using ELISA), proliferation of T cells (using liquid scintillation counter), and cytotoxicity (using MTT assay)). The methanolic extract of Distemonanthus benthamianus inhibited protein denaturation (75.63%) and the activities of cyclooxygenase (78.92%) and 5-lipoxygenase (81.54%). The extract also significantly ( p < 0.001 ) inhibited intracellular and extracellular ROS production and T cell proliferation and reduced significantly ( p < 0.01 , p < 0.001 ) TNF-α, IL-1β, IL-6, and PGE2 production. At all doses (125, 250, and 500 mg/kg), the extract significantly reduces the ulceration index and the area of ulceration and significantly increases the mass of gastric mucus. In addition, the extract significantly decreases the level of MDA, significantly increases the activities of catalase and glutathione, and then improves the hematological parameters in sick animals. Histological micrographs show that in the presence of the extract, there is advanced reepithelialization with recovery of the ulcerated epithelium. Thus, the extract of Distemonanthus benthamianus has healing properties against gastric ulcers which are associated with its anti-inflammatory, immunomodulatory, and antioxidant effects.

scholarly journals Avβ3 Single-Stranded DNA Aptamer Attenuates Vascular Smooth Muscle Cell Proliferation and Migration via Ras-PI3K/MAPK Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Hong-Bing Wu ◽  
Zhi-Wei Wang ◽  
Feng Shi ◽  
Zong-Li Ren ◽  
Luo-Cheng Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cell Cycle Progression ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Dna Aptamer ◽  
Mitogen Activated Protein Kinase ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Objectives. To observe the effect of avβ3 single-stranded (ss) DNA on proliferation and migration of vascular smooth muscle cells (VSMCs) and its potential mechanism. Background. Percutaneous transluminal coronary angioplasty (PTCA) is currently the preferred method for the treatment of coronary heart disease. However, vascular restenosis still occurs after PTCA treatment, severely affecting the clinical efficacy of PTCA. Integrin avβ3, which is widely expressed on various cell surfaces, plays an important role in the proliferation and migration of VSMCs. Methods. In this experiment, we used systematic evolution of ligands by exponential enrichment (SELEX) to screen out avβ3 ssDNA, which has high affinity and specificity to the avβ3 protein. MTT, Transwell, and cell scratch assays were carried out to examine the effect of avβ3 ssDNA on the proliferation and migration of VSMCs. Flow cytometry was performed to detect apoptosis and cell cycle progression. The effect of avβ3 ssDNA on the Ras-phosphatidylinositol-4,5-bisphosphate 3-kinase/mitogen-activated protein kinase (PI3K/MAPK) signaling pathway was evaluated by quantitative reverse transcription polymerase chain reaction and western blot. Results. In the present study, we found that avβ3 ssDNA significantly decreased the expression of osteopontin, focal adhesion kinase, Ras, p-PI3K, and p-MAPK at both mRNA and protein levels (P<0.05). Avβ3 ssDNA also inhibited VSMC proliferation and migration while promoting apoptosis (P<0.05), as demonstrated by the upregulation of the proapoptotic proteins Bax and active caspase 3 (P<0.05). Conclusions. The findings suggest that avβ3 ssDNA inhibited the proliferation and migration of VSMCs by suppressing the activation of Ras-PI3K/MAPK signaling.

TMEM98, a novel secretory protein, promotes endothelial cell adhesion as well as vascular smooth muscle cell proliferation and migration

2020 ◽  
Author(s):  
Mei Li ◽  
Hongmei Zhu ◽  
Xiaoyan Hu ◽  
Fuhua Gao ◽  
Xinxin Hu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Transmembrane Protein ◽  
Vsmc Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Transmembrane protein 98 (TMEM98) is a novel gene. In a prior study, we have shown that siRNA-mediated knockdown of TMEM98 inhibited interleukin (IL)-8-promoted endothelial cell (EC) adhesion as well as vascular smooth muscle cell (VSMC) proliferation and migration in the vascular endothelial and smooth muscle cells dysfunction. Herein, we used gain- and loss-of-function approaches combined with biochemical techniques to further explore the role of TMEM98 in the vascular wall cell. The expression and secretion of TMEM98 was increased in cultured human umbilical vein endothelial cells (HUVECs) and VSMCs treated with IL-8 and platelet-derived growth factor (PDGF)-BB. Also, PDGF-BB secretion was increased in TMEM98-treated HUVECs and VSMCs. Thus, it appears that TMEM98 and PDGF-BB form a positive feedback loop in potentiation of EC adhesion as well as VSMC proliferation and migration. Knockdown of TMEM98 mediated by siRNA inhibited PDGF-BB-promoted EC adhesion by downregulating the expression of ICAM-1 and VCAM-1 as well as impaired the proliferation and migration of VSMCs through suppressing the AKT/GSK3β/cyclin D1 signaling pathway and reducing the expression of β-catenin. Hence, TMEM98 promoted EC adhesion through inducing the expression of ICAM-1/VCAM-1 and triggered VSMC proliferation and migration through activating the ERK and AKT/GSK3β signaling pathways. Taken together, TMEM98 may serve as a potential therapeutic target for the clinical treatment.

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