Atherosclerosis

2000

DOI: 10.1016/s0021-9150(99)00371-8

|View full text |Cite

|

Sign up to set email alerts

|

Atherosclerotic arterial remodeling and the localization of macrophages and matrix metalloproteases 1, 2 and 9 in the human coronary artery

Gérard Pasterkamp¹,

Arjan H. Schoneveld²,

DirkJan Hijnen³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Discussion3

The Effects Of Antiatherosclerotic Drugs1

Citation Types

Supporting

12

Mentioning

183

Contrasting

0

Unclassified

10

Year Published

2003

2003

2014

2014

Publication Types

Select...

Article9

Other1

Relationship

Self Cite0

Independent10

Authors

Journals

Cited by 292 publications

(205 citation statements)

References 27 publications

Supporting

12

Mentioning

183

Contrasting

0

Unclassified

10

Order By: Relevance

“…Among MMPs, MMP-2 and MMP-9 represent the gelatinase group and are of particular interest in atherosclerosis due to their significant roles in the regulation of VSMC proliferation and migration. It has been shown that MMP-2 is constitutively expressed in VSMCs in normal arteries in addition to increased MMP-2 expression, and MMP-9 expression is induced in VSMCs and macrophages in atherosclerotic arteries (26). In this study, we found that TNF-α enhanced MMP-2 and MMP-9 mRNA and protein expression in Figure 5.…”

Section: Discussionsupporting

confidence: 56%

Emodin inhibits tumor necrosis factor-α-induced migration and inflammatory responses in rat aortic smooth muscle cells

¹

,

²

,

³

et al. 2012

Int J Mol Med

View full text Add to dashboard Cite

Abstract. Emodin, a naturally occurring anthraquinone derivative in oriental herbal medicine, has been shown to exert a variety of pharmacological activities. The goal of this study was to determine the effects of emodin on the modulation of cell proliferation, migration, inflammatory responses, and matrix metalloproteinase (MMP)-2 and MMP-9 expression in tumor necrosis factor (TNF)-α-induced rat aortic smooth muscle cells (RASMCs). Cell proliferation and migration were measured using the MTT assay and the transwell chamber assay, respectively. Quantitative real-time PCR and western blot analysis were used to detect MMP expression. Gel shift was used for analysis of nuclear factor (NF)-κB activation. In addition, the expression of several inflammatory genes was also analyzed. Treatment of RASMCs with emodin significantly and dose-dependently attenuated TNF-α-induced proliferation, migration, mRNA and protein expression of MMP-2 and MMP-9, and NF-κB activation. Furthermore, emodin significantly inhibited TNF-α-evoked inflammatory responses, as demonstrated by the reduction in the expression of inflammatory genes. These results suggest that emodin inhibits TNF-α-induced proliferation, migration, MMP-2 and MMP-9 expression as well as inflammatory responses in cultured RASMCs, supporting the notion that emodin may have potential application in clinical atherosclerosis disease.

“…Among MMPs, MMP-2 and MMP-9 represent the gelatinase group and are of particular interest in atherosclerosis due to their significant roles in the regulation of VSMC proliferation and migration. It has been shown that MMP-2 is constitutively expressed in VSMCs in normal arteries in addition to increased MMP-2 expression, and MMP-9 expression is induced in VSMCs and macrophages in atherosclerotic arteries (26). In this study, we found that TNF-α enhanced MMP-2 and MMP-9 mRNA and protein expression in Figure 5.…”

Section: Discussionsupporting

confidence: 56%

Emodin inhibits tumor necrosis factor-α-induced migration and inflammatory responses in rat aortic smooth muscle cells

¹

,

²

,

³

et al. 2012

Int J Mol Med

View full text Add to dashboard Cite

Abstract. Emodin, a naturally occurring anthraquinone derivative in oriental herbal medicine, has been shown to exert a variety of pharmacological activities. The goal of this study was to determine the effects of emodin on the modulation of cell proliferation, migration, inflammatory responses, and matrix metalloproteinase (MMP)-2 and MMP-9 expression in tumor necrosis factor (TNF)-α-induced rat aortic smooth muscle cells (RASMCs). Cell proliferation and migration were measured using the MTT assay and the transwell chamber assay, respectively. Quantitative real-time PCR and western blot analysis were used to detect MMP expression. Gel shift was used for analysis of nuclear factor (NF)-κB activation. In addition, the expression of several inflammatory genes was also analyzed. Treatment of RASMCs with emodin significantly and dose-dependently attenuated TNF-α-induced proliferation, migration, mRNA and protein expression of MMP-2 and MMP-9, and NF-κB activation. Furthermore, emodin significantly inhibited TNF-α-evoked inflammatory responses, as demonstrated by the reduction in the expression of inflammatory genes. These results suggest that emodin inhibits TNF-α-induced proliferation, migration, MMP-2 and MMP-9 expression as well as inflammatory responses in cultured RASMCs, supporting the notion that emodin may have potential application in clinical atherosclerosis disease.

“…Indeed, MMP-9 was highly expressed in the shoulder regions of advanced atherosclerotic lesions (Galis et al, 1994;Brown et al, 1995). Its concentration and activity were significantly higher in unstable atheroseclerotic plaque with intense inflammatory cell infiltration, hence contributing to the plaque rupture ultimately (Loftus et al, 2000;Pasterkamp et al, 2000). Some cross-sectional studies have reported that the plasma MMP-9 level was significantly higher in CAD patients, in particular in acute MI, than in control subjects (Kai et al, 1998;Tayebjee et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Association of matrix metalloproteinase-9 C1562T polymorphism and coronary artery disease: a meta-analysis

¹

,

²

2014

J. Zhejiang Univ. Sci. B

View full text Add to dashboard Cite

Abstract:Objective: Many investigations have studied the associations between matrix metalloproteinase-9 (MMP-9) C1562T polymorphisms and coronary artery disease (CAD). However, the conclusions of these studies were inconsistent. Therefore, this study was aimed at clarifying the association between MMP-9 C1562T polymorphisms and CAD in a large-scale meta-analysis. Methods: The PubMed and Embase databases were retrieved to collect all publications on the association between MMP-9 C1562T polymorphisms and CAD. Then the odd ratios (ORs) and 95% confidence intervals (95% CIs) for C1562T TT+TC versus CC genotype between CAD and the control groups were evaluated. Subgroup analysis was also performed according to different races. The meta-analysis was performed by Stata 10.0. Results: Sixteen case-control studies were included in our meta-analysis, involving 11 032 CAD patients and 4628 non-CAD controls. Compared with C allele carriers, East Asian T allele carriers TT+TC had a significantly higher risk of CAD (OR=1.43; 95% CI: 1.03-1.99; P=0.031); however, there were no significant associations in Western populations (OR=1.06; 95% CI: 0.96-1.18; P=0.240) or West Asians (OR=1.13; 95% CI: 0.75-1.70; P=0.565). When further analyzing the association between C1562T polymorphisms and myocardial infarction (MI, the most serious type of CAD), the risk of TT+TC genotype versus CC genotype for MI was significantly higher for the overall (OR=1.21; 95% CI: 1.04-1.40; P=0.012) and for East Asians (OR=1.58; 95% CI: 1.26-1.97; P=0.000) but not in Western populations (OR=1.12; 95% CI: 0.99-1.26; P=0.078). Conclusions: Our meta-analysis suggested an obvious ethnic difference in the association between MMP-9 C1562T polymorphisms and CAD. MMP-9 C1562T polymorphism was significantly related to CAD in East Asians. However, no significant associations were observed in either West Asians or Western populations.

“…(28) Members of the MMP family have also been identified in human atherosclerotic plaque shoulders and in regions of foam cell accumulation, contributing to lesion progression, plaque vulnerability, and de novo atherosclerotic remodeling. (29) In addition, expression of serum MMPs has been found in patients with acute coronary syndrome and osteoporosis. (30,31) These data suggest that chronic inflammation, inflammatory markers, and MMPs might play pivotal roles in the relationship between osteoporotic hip fracture and subsequent AMI.…”

Section: Discussionmentioning

confidence: 99%

Hip fracture and risk of acute myocardial infarction: A nationwide study

¹

,

²

,

³

et al. 2012

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

Osteoporotic fractures are associated with increased mortality risk. However, little data are available on the risk of acute myocardial infarction (AMI) after hip fracture. Therefore, we investigated whether hip fracture increased the risk of AMI in a large, nationwide cohort study. We obtained data from 8758 patients diagnosed with hip fracture from 2000 to 2009 and from 4 matched controls for each patient from the Longitudinal Health Insurance Database (LHID 2000), Taiwan. Controls were matched for age, sex, comorbid disorders, and enrollment date. All subjects were followed up from the date of enrollment until AMI, death, or the end of data collection (2009). Cox's regression model adjusted for age, sex, comorbid disorders, and medication was used to assess independent factors determining the risk of development of AMI. As expected, despite the matching, the hip fracture patients had more risk factors for AMI at baseline. A total of 8758 subjects with hip fractures and 35,032 controls were identified. Among these patients, 1183 (257 hip fracture patients and 926 controls) developed AMI during the median 3.2-year (interquartile range 1.4 to 5.8 years) follow-up period. Patients with hip fractures had a higher incidence of AMI occurrence when compared with controls (8.7/1000 person-years versus 6.82/1000 person-years). Multivariate analysis adjusted for baseline covariates indicated that hip fracture was associated with a greater risk for AMI development (hazard ratio [HR] ¼ 1.29; 95% confidence interval [CI] 1.12-1.48; p < 0.001). We conclude that hip fracture is independently associated with a higher risk of subsequent AMI. ß

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2024 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.