scholarly journals Lysophosphatidic Acid Is Associated with Atherosclerotic Plaque Instability by Regulating NF-κB Dependent Matrix Metalloproteinase-9 Expression via LPA2 in Macrophages

2017 ◽  
Vol 8 ◽  
Author(s):  
Chun Gu ◽  
Fang Wang ◽  
Zhenwen Zhao ◽  
Hongyue Wang ◽  
Xiangfeng Cong ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Atherosclerotic Plaque ◽  
Lysophosphatidic Acid ◽  
Matrix Metalloproteinase 9 ◽  
Plaque Instability ◽  
Metalloproteinase 9

scholarly journals The Role of Matrix Metalloproteinase-9 in Atherosclerotic Plaque Instability

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Tiewei Li ◽  
Xiaojuan Li ◽  
Yichuan Feng ◽  
Geng Dong ◽  
Yuewu Wang ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Atherosclerotic Plaque ◽  
Predictive Biomarker ◽  
Matrix Metalloproteinase 9 ◽  
Atherosclerotic Plaques ◽  
Plaque Instability ◽  
Cerebrovascular Events ◽  
Plaque Inflammation ◽  
Metalloproteinase 9

Matrix metalloproteinase-9 (MMP-9) belongs to the MMP family and has been widely investigated. Excessive MMP-9 expression can enhance extracellular matrix degradation and promote plaque instability. Studies have demonstrated that MMP-9 levels are higher in vulnerable plaques than in stable plaques. Additionally, several human studies have demonstrated that MMP-9 may be a predictor of atherosclerotic plaque instability and a risk factor for future adverse cardiovascular and cerebrovascular events. MMP-9 deficiency or blocking MMP-9 expression can inhibit plaque inflammation and prevent atherosclerotic plaque instability. All of these results suggest that MMP-9 may be a useful predictive biomarker for vulnerable atherosclerotic plaques, as well as a therapeutic target for preventing atherosclerotic plaque instability. In this review, we describe the structure, function, and regulation of MMP-9. We also discuss the role of MMP-9 in predicting and preventing atherosclerotic plaque instability.

scholarly journals Levels of Matrix Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinase-1 mRNAs in Patients with Primary Hypertension or Hypertension-Induced Atherosclerosis

2012 ◽  
Vol 40 (3) ◽  
pp. 986-994 ◽  
Author(s):  
W Su ◽  
F Gao ◽  
J Lu ◽  
W Wu ◽  
G Zhou ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Atherosclerotic Plaque ◽  
Matrix Metalloproteinase 9 ◽  
Primary Hypertension ◽  
Mrna Levels ◽  
Tissue Inhibitor ◽  
Hypertensive Patients ◽  
Matrix Metalloproteinase 1 ◽  
Normotensive Subjects ◽  
Metalloproteinase 9

OBJECTIVE: Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) affect degradation of vascular elastin, collagen remodelling and formation of atherosclerotic plaque. This cross-sectional study investigated the levels of MMP-9 and TIMP-1 mRNAs in the blood of patients with primary hypertension with and without hypertension-induced carotid atherosclerosis. METHODS: Hypertensive patients with and without atherosclerosis and age- and gender-matched normotensive subjects were enrolled. MMP-9 and TIMP-1 mRNA were quantified using real-time reverse transcription—polymerase chain reaction. RESULTS: Hypertensive patients ( n = 86) had significantly lower levels of TIMP-1 mRNA than normotensive subjects ( n = 43). Hypertensive patients with atherosclerosis ( n = 42) showed significantly elevated levels of MMP-9 mRNA compared with both normotensive subjects and hypertensive patients without atherosclerosis ( n = 44). CONCLUSIONS: Primary hypertension resulted in decreased TIMP-1 mRNA levels, suggesting a potential mechanism contributing to the degradation of elastin. Hypertension-induced atherosclerosis was associated with significantly increased levels of MMP-9 mRNA, which may enhance both the deposition of types I and III collagen and atherosclerotic plaque formation.

Expression of matrix metalloproteinase 9 and its regulators in the unstable coronary atherosclerotic plaque

2005 ◽  
Author(s):  
Fei Chen ◽  
Per Eriksson ◽  
Göran Hansson ◽  
Istvan Herzfeld ◽  
Magareta Klein ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Atherosclerotic Plaque ◽  
Matrix Metalloproteinase 9 ◽  
Coronary Atherosclerotic Plaque ◽  
Metalloproteinase 9

scholarly journals Epigallocatechin-3-Gallate Inhibits Matrix Metalloproteinase-9 and Monocyte Chemotactic Protein-1 Expression Through the 67-κDa Laminin Receptor and the TLR4/MAPK/NF-κB Signalling Pathway in Lipopolysaccharide-Induced Macrophages

2017 ◽  
Vol 43 (3) ◽  
pp. 926-936 ◽  
Author(s):  
Ya-Fei Li ◽  
Hao Wang ◽  
Yi Fan ◽  
Hao-jie Shi ◽  
Qi-Ming Wang ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Signalling Pathway ◽  
Negative Regulator ◽  
Laminin Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Plaque Instability ◽  
Monocyte Chemotactic Protein ◽  
Chemotactic Protein ◽  
Metalloproteinase 9

Background/Aims: Epigallocatechin-3-gallate (EGCG), a major catechin found in green tea, has been shown to prevent cardiovascular diseases. Previously, Matrix metalloproteinase-9 (MMP-9), monocyte chemotactic protein-1 (MCP-1) and toll-like receptor 4 (TLR4) were confirmed to play an important role in atherosclerosis and plaque instability. Both TLR4 and its negative regulator, Toll-interacting protein (Tollip), could be mediated by EGCG. The present study aimed to examine the effect of physiological concentration of EGCG (1 µM) on the expression of MMP-9 and MCP-1 in lipopolysaccharide (LPS)-induced macrophages and the potential mechanisms underlying its actions. Methods: The RAW264.7 cell line was used. Western blot was used to determine MCP-1, TLR4, Tollip, Mitogen-activated protein kinase (MAPK) and Nuclear factor-κB (NF-κB) protein expression. MMP-9 activity was assayed by gelatine zymography. The mRNA expression of MMP-9 and MCP-1 was measured by realtime polymerase chain reaction (RT-PCR). Results: EGCG (1 µM) significantly suppressed the expression of MMP-9 and MCP-1 and inhibited MAPK and NF-κB in LPS-induced macrophages but was blocked by Tollip silencing. The expression of LPS-induced MMP-9 and MCP-1 and the phosphorylation of the ERK1/2, P38 and NF-κB pathway proteins decreased after TLR4 siRNA treatment. Furthermore, EGCG mediated TLR4 and Tollip expression through binding to 67-kDa laminin receptor (67LR). Conclusion: The results of our study suggested that EGCG (1 µM) suppresses the TLR4/MAPK/NF-κB signalling pathway, decreases the expression of the plaque instability-mediating cytokines MMP-9 and MCP-1, and might prove to be effective in stabilizing atherosclerotic plaque.

Matrix metalloproteinase-9 expression in carotid atherosclerotic plaque and contrast-enhanced MRI in a swine model

2012 ◽  
Vol 6 (1) ◽  
pp. 24-28 ◽  
Author(s):  
Xiao-Bing Jiang ◽  
Wei-Si Yuan ◽  
Jin-Shan Wang ◽  
Zhong Liu ◽  
Dong-Hong Liu ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Atherosclerotic Plaque ◽  
Matrix Metalloproteinase 9 ◽  
Swine Model ◽  
Carotid Atherosclerotic Plaque ◽  
Enhanced Mri ◽  
Contrast Enhanced ◽  
Metalloproteinase 9 ◽  
Contrast Enhanced Mri
Sign in / Sign up

Export Citation Format

Share Document