Platelet-derived growth factor-BB induces matrix metalloproteinase-2 expression and rat vascular smooth muscle cell migration via ROCK and ERK/p38 MAPK pathways

Cui, Ying; Sun, Yin-Wei; Lin, Haishuang; Su, Weimin; Yan, Fang; Zhao, Ying; Xin, Wei; Qin, Yuanhua; Kohama, Kazuhiro; Gao, Ying

doi:10.1007/s11010-014-2068-5

Cited by 50 publications

(36 citation statements)

References 28 publications

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“…PDGF, mainly expressed in VSMCs and endothelial cells, promote mitosis and play an important role in the proliferation of VSMCs [6][7][8]37]. The binding of PDGF-BB, a subtype of PDGF released from injured vessels, to its receptor can trigger the activation of downstream and then contribute significantly to VSMCs proliferation [9][10][11][12]. In this paper, PDGF-BB could effectively induce MOVAS proliferation, which was consistent with the previous studies reported.…”

Section: Discussionsupporting

confidence: 87%

“…Compared with DMSO treated group, the expression levels of PCNA and Ki67 were significantly increased in PDGF-BB induced MOVAS cells, but this increment was dampened by OMT treatment ( Figure 2C). (0,5,10,20,40 …”

Section: Resultsmentioning

confidence: 99%

“…Platelet-Derived Growth Factor (PDGF) is an important regulator that stimulates the proliferation of VSMCs [6][7][8]. The binding of PDGF-BB, a subtype of PDGF, to its receptor triggers the activation of downstream signaling molecules such as Mitogen-Activated Protein Kinases (MAPKs) to promote VSMCs proliferation and growth [9][10][11][12][13]. Therefore, preventing the PDGF-BB induced VSMCs proliferation might be a promising strategy for treating the development of neointima in atherosclerosis and post-angioplasty restenosis in the future.…”

Section: Introductionmentioning

confidence: 99%

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Oxymatrine suppresses MOVAS proliferation induced by platelet-derived growth factor via G0/G1 arrest

Li¹,

Hu²,

Gao³

et al. 2018

biomedicalresearch

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Objective: The traditional Chinese medicine Oxymatrine (OMT) has numerous biological effects, such as anti-inflammatory, anti-fibrosis, anti-proliferation and anti-tumor. However, the underlying effect of OMT on vascular smooth muscle cells remains unclear. Herein, the aim of this study is to investigate the role and mechanism of OMT on MOVAS (a mouse vascular aortic smooth muscle cell line) proliferation induced by Platelet-Derived Growth Factor-BB (PDGF-BB). Methods: Firstly, we assessed proliferation in MOVAS subjected to PDGF-BB induction or controlled intervention with/without OMT treatment. And then we detected cell cycle, cell apoptosis and the expression levels of cyclins, Cyclin-Dependent Kinases (CDKs) and p21 of each group. Results: In the present study, we found that OMT remarkably restrained the proliferation induced by PDGF-BB stimulus. Additionally, it was demonstrated that cell population of MOVAS treated with OMT in the S phase was reduced, but that of MOVAS in the G0/G1 phase was increased when compared to the PDGF-BB group. However, OMT treatment showed no effect on MOVAS apoptosis. Mechanistically, the expression of cyclinD1-CDK4/6 and cyclinE2-CDK2 were inhibited, while the expression of p21 was increased in MOVAS treated with OMT. Conclusion: These results demonstrated that the inhibitory effect of OMT on proliferation of MOVAS were in part due to G 0 /G 1 arrest by inhibiting cyclinD1-CDK4/6 and cyclinE2-CDK2, and promoting p21 expression. Therefore, OMT might become a new strategy for treating excessive proliferation of vascular smooth muscle cells in the future.

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Section: Discussionsupporting

confidence: 87%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxymatrine suppresses MOVAS proliferation induced by platelet-derived growth factor via G0/G1 arrest

Li¹,

Hu²,

Gao³

et al. 2018

biomedicalresearch

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show abstract

“…PDGF stimulates the production of MMP-2 by SMCs and enable the migration of medial SMCs into the intima. 20,36 Moreover, MMP-2 has been associated previously with a more stable plaque phenotype, whereas a high expression of MMP-1, MMP-8, and MMP-9 is associated with more vulnerable plaques. 37,38 MMP3, among other types of proteinases, has been implicated in cleaving pro-HB-EGF to release the mature form of HB-EGF.…”

Section: Discussionmentioning

confidence: 97%

High Plasma Levels of Heparin-Binding Epidermal Growth Factor Are Associated With a More Stable Plaque Phenotype and Reduced Incidence of Coronary Events

Rattik

Wigren

Björkbacka

et al. 2015

ATVB

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Objective-Rupture of atherosclerotic plaques is the major cause of acute coronary events (CEs). Plaque destabilization is the consequence of an imbalance between inflammatory-driven degradation of fibrous tissue and smooth muscle celldependent tissue repair. Proinflammatory factors have been documented extensively as biomarkers of cardiovascular risk but factors that contribute to stabilization of atherosclerotic plaques have received less attention. The present study aimed to investigate whether plasma levels of the smooth muscle cell growth factor epidermal growth factor (EGF), heparinbinding-EGF (HB-EGF), and platelet-derived growth factor correlate with plaque phenotype and incidence of CEs. Approach and Results-HB-EGF, EGF and platelet-derived growth factor were measured in plasma from 202 patients undergoing carotid endarterectomy and in 384 incident CE cases and 409 matched controls recruited from the Malmö Diet and Cancer cohort. Significant positive associations were found between the plasma levels of all 3 growth factors and the collagen and elastin contents of the removed plaques. CE cases in the Malmö Diet and Cancer cohort had lower levels of HB-EGF in plasma, whereas no significant differences were found for EGF and platelet-derived growth factor. After adjusting for cardiovascular risk factors in a Cox proportional hazard model, the hazard ratio for the highest HB-EGF tertile was 0.61 (95% confidence interval, 0.47-0.82; P<0.001). Conclusions-The associations between high levels of smooth muscle cell growth factors in plasma and a more fibrous plaque phenotype as well as the association between low levels of HB-EGF and incident CEs point to a potential clinically important role for factors that contribute to plaque stabilization by stimulating smooth muscle cells.

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“…For example, overexpression of VEGFa in SNU-5 cells increases MMP-2 expression, whereas downregulation of VEGFa decreases MMP-2 expression (Mao et al, 2014). Also, platelet-derived growth factor-BB increases MMP-2 expression in rat VSMCs, possibly via Rho-associated protein kinase, extracellular signal-regulated kinases, and p38 MAPK phosphorylation (Cui et al, 2014). Also, in a study on carotid plaques, epidermal growth factor (EGF) upregulated MMP-9 activity and increased MMP-1, -9, and EGF receptor (EGFR) mRNA transcripts in VSMCs (Rao et al, 2014).…”

Section: Mmps and Vsm Dysfunction In Vvsmentioning

confidence: 99%

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

MacColl

Khalil

2015

J Pharmacol Exp Ther

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Lower-extremity veins have efficient wall structure and function and competent valves that permit upward movement of deoxygenated blood toward the heart against hydrostatic venous pressure. Matrix metalloproteinases (MMPs) play an important role in maintaining vein wall structure and function. MMPs are zinc-binding endopeptidases secreted as inactive pro-MMPs by fibroblasts, vascular smooth muscle (VSM), and leukocytes. ProMMPs are activated by various activators including other MMPs and proteinases. MMPs cause degradation of extracellular matrix (ECM) proteins such as collagen and elastin, and could have additional effects on the endothelium, as well as VSM cell migration, proliferation, Ca 21 signaling, and contraction. Increased lower-extremity hydrostatic venous pressure is thought to induce hypoxia-inducible factors and other MMP inducers/ activators such as extracellular matrix metalloproteinase inducer, prostanoids, chymase, and hormones, leading to increased MMP expression/activity, ECM degradation, VSM relaxation, and venous dilation. Leukocyte infiltration and inflammation of the vein wall cause further increases in MMPs, vein wall dilation, valve degradation, and different clinical stages of chronic venous disease (CVD), including varicose veins (VVs). VVs are characterized by ECM imbalance, incompetent valves, venous reflux, wall dilation, and tortuosity. VVs often show increased MMP levels, but may show no change or decreased levels, depending on the VV region (atrophic regions with little ECM versus hypertrophic regions with abundant ECM) and MMP form (inactive pro-MMP versus active MMP). Management of VVs includes compression stockings, venotonics, and surgical obliteration or removal. Because these approaches do not treat the causes of VVs, alternative methods are being developed. In addition to endogenous tissue inhibitors of MMPs, synthetic MMP inhibitors have been developed, and their effects in the treatment of VVs need to be examined.

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Platelet-derived growth factor-BB induces matrix metalloproteinase-2 expression and rat vascular smooth muscle cell migration via ROCK and ERK/p38 MAPK pathways

Cited by 50 publications

References 28 publications

Oxymatrine suppresses MOVAS proliferation induced by platelet-derived growth factor via G0/G1 arrest

Oxymatrine suppresses MOVAS proliferation induced by platelet-derived growth factor via G0/G1 arrest

High Plasma Levels of Heparin-Binding Epidermal Growth Factor Are Associated With a More Stable Plaque Phenotype and Reduced Incidence of Coronary Events

Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease

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