The Extracellular Matrix Metalloproteinase Inducer (EMMPRIN, CD147) - a potential novel target in atherothrombosis prevention?

Joghetaei, Nader; Stein, Andreas; Byrne, Robert A.; Schulz, Christian; King, Lamin; May, Andreas E.; Schmidt, Roland

doi:10.1016/j.thromres.2013.04.017

Cited by 23 publications

(19 citation statements)

References 47 publications

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“…In this study, we found that green tea polyphenol EGCG significantly inhibited the expression and activity of MMP-9 in a concentration-dependent manner in PMA-induced macrophages. More importantly, EGCG also inhibited the expression of EMMPRIN, which can induce the synthesis of MMPs and has recently been implicated in the development of atherosclerosis and atherothrombosis [14]. Moreover, downregulation of EMMPRIN significantly inhibited MMP-9 expression and enzymatic activity in PMA-induced macrophages, suggesting that EMMPRIN plays a key role in the inhibitory effects of EGCG on MMP-9 expression and activity.…”

Section: Discussionmentioning

confidence: 87%

“…Furthermore, overexpression of EMMPRIN was observed in inflammatory disease such as lung inflammatory disease, rheumatoid arthritis and chronic liver disease [11][12][13]. In recent years, a significant amount of evidence has documented the pivotal role of EMMPRIN in the complex processes of atherosclerosis and acute atherosclerothrombosis [14]. EMMPRIN was reported overexpressed in human atherosclerotic plaques, and was colocalized with macrophages/monocytes [15].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of EMMPRIN and MMP-9 Expression by Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor in PMA-Induced Macrophages

Wang

et al. 2016

Cell Physiol Biochem

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Background/Aims: It is well documented that overexpression of EMMPRIN (extracellular matrix metalloproteinase inducer) and MMPs (matrix metalloproteinases) by monocytes/macrophages plays an important role in atherosclerotic plaque rupture. Green tea polyphenol epigallocatechin-3-gallate (EGCG) has a variety of pharmacological properties and exerts cardiovascular protective effects. Recently, the 67-kD laminin receptor (67LR) has been identified as a cell surface receptor of EGCG. The aim of the present study was to evaluate the effects of EGCG on the expression of EMMPRIN and MMP-9 in PMA-induced macrophages, and the potential mechanisms underlying its effects. Methods: Human monocytic THP-1 cells were induced to differentiate into macrophages with phorbol 12-myristate 13-acetate (PMA). Protein expression and MMP-9 activity were assayed by Western blot and Gelatin zymography, respectively. Real-time PCR was used to examine EMMPRIN and MMP-9 mRNA expression. Results: We showed that EGCG (10-50µmol/L) significantly inhibited the expression of EMMPRIN and MMP-9 and activation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38 and c-Jun N-terminal kinase (JNK) in PMA-induced macrophages. Downregulation of EMMPRIN by gene silencing hindered PMA-induced MMP-9 secretion and expression, indicating an important role of EMMPRIN in the inhibition of MMP-9 by EGCG. Moreover, 67LR was involved in EGCG-mediated suppression of EMMPRIN and MMP-9 expression. Anti-67LR antibody treatment led to abrogation of the inhibitory action of EGCG on the expression of EMMPRIN and MMP-9 and activation of ERK1/2, p38, and JNK. Conclusion: Our results indicate that EGCG restrains EMMPRIN and MMP-9 expression via 67LR in PMA-induced macrophages, which also suggests that EGCG may be a possible therapeutic agent for stabilizing atherosclerotic plaque.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Inhibition of EMMPRIN and MMP-9 Expression by Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor in PMA-Induced Macrophages

Wang

et al. 2016

Cell Physiol Biochem

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“…VEGF, a pro-angiogenic growth factor, has been found correlated closely with neovessels within atherosclerotic plaques, macrophage accumulation, and plaque instability. 7,9,10 CD147, also called Extracellular Matrix Metalloproteinase Inducer(EMMPRIN), which was originally discovered on the surface of solid tumor cells, has been found the ability to promote the angiogenesis in many pathological conditions such as cancer diseases and rheumatoid arthritis via the up-regulation of VEGF [11][12][13] .Since CD147 is also discovered to play a pivotal role in the complex processes of atherogenesis and acute plaque rupture and thrombosis [14][15][16][17] , we hypothesis that CD147 would also induce the up-regulation of VEGF in foam cells formation in atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

CD147 induces up-regulation of vascular endothelial growth factor in U937-derived foam cells through PI3K/AKT pathway

Zong

et al. 2016

Archives of Biochemistry and Biophysics

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“…CD147 plays an important role in a number of organ systems, including the Ok blood group [118], cardiovascular system [119,120], nervous system [121], and T cells of the immune system [122]. CD147 is expressed in epithelial cells [99], fibroblasts [123], psoriatic peripheral blood mononuclear cells [124], cytotrophoblasts [125], the normal basal epithelial layer reportedly harboring stem cells [126], ectopic endometrial tissues [127], systemic lupus erythematosus [128], synovial joint disease tissue of rheumatoid arthritis (RA) patients [115,129], plasma of lupus nephritis patients [130], peripheral monocytes and T lymphocytes of patients with ankylosing spondylitis [131].…”

Section: The Expression and Role Of Cd147 In Tissues And Diseases mentioning

confidence: 99%

The Biological Function and Clinical Utilization of CD147 in Human Diseases: A Review of the Current Scientific Literature

Xiong

Edwards

Zhou

2014

IJMS

186

194

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CD147 or EMMPRIN is a member of the immunoglobulin superfamily in humans. It is widely expressed in human tumors and plays a central role in the progression of many cancers by stimulating the secretion of matrix metalloproteinases (MMPs) and cytokines. CD147 regulates cell proliferation, apoptosis, and tumor cell migration, metastasis and differentiation, especially under hypoxic conditions. CD147 is also important to many organ systems. This review will provide a detailed overview of the discovery, characterization, molecular structure, diverse biological functions and regulatory mechanisms of CD147 in human physiological and pathological processes. In particular, recent studies have demonstrated the potential application of CD147 not only as a phenotypic marker of activated regulatory T cells but also as a potential diagnostic marker for early-stage disease. Moreover, CD147 is recognized as an effective therapeutic target for hepatocellular carcinoma (HCC) and other cancers, and exciting clinical progress has been made in HCC treatment using CD147-directed monoclonal antibodies.

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The Extracellular Matrix Metalloproteinase Inducer (EMMPRIN, CD147) - a potential novel target in atherothrombosis prevention?

Cited by 23 publications

References 47 publications

Inhibition of EMMPRIN and MMP-9 Expression by Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor in PMA-Induced Macrophages

Inhibition of EMMPRIN and MMP-9 Expression by Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor in PMA-Induced Macrophages

CD147 induces up-regulation of vascular endothelial growth factor in U937-derived foam cells through PI3K/AKT pathway

The Biological Function and Clinical Utilization of CD147 in Human Diseases: A Review of the Current Scientific Literature

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