AVISCERA BIOSCIENCE
| CD147/EMMPRIN (Soluble) (Human) ELISA Kit | |
| CD147/EMMPRIN is a biomarker for cancer research | |
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Pathogenic Neisseria meningitidis utilizes CD147 for vascular colonization |
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| Neisseria meningitidis is a cause of meningitis epidemics worldwide and of rapidly progressing fatal septic shock. A crucial step in the pathogenesis of invasive meningococcal infections is the adhesion of bloodborne meningococci to both peripheral and brain endothelia, leading to major vascular dysfunction. Initial adhesion of pathogenic strains to endothelial cells relies on meningococcal type IV pili, but the endothelial receptor for bacterial adhesion remains unknown. Here, we report that the immunoglobulin superfamily member CD147 (also called extracellular matrix metalloproteinase inducer (EMMPRIN) or Basigin) is a critical host receptor for the meningococcal pilus components PilE and PilV. Interfering with this interaction potently inhibited the primary attachment of meningococci to human endothelial cells in vitro and prevented colonization of vessels in human brain tissue explants ex vivo and in humanized mice in vivo. These findings establish the molecular events by which meningococci target human endothelia, and they open new perspectives for treatment and prevention of meningococcus-induced vascular dysfunctions. | |
| Bernard SC et al. Nat Med. 2014 Jun 1. doi: 10.1038/nm.3563. [Epub ahead of print] | |
Circulating levels of soluble EMMPRIN (CD147) correlate with levels of soluble glycoprotein VI in human plasma |
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| Abstract Extracellular matrix metalloproteinase inducer (EMMPRIN; CD147), which binds to the platelet-specific collagen receptor glycoprotein (GP) VI, is expressed in a range of cell types including platelets and leukocytes, and has been implicated in neoplastic disease and atherosclerotic coronary disease. Both CD147 and GPVI can be shed from cell membranes and detected in plasma. However, while the relationship between soluble CD147 (sCD147), soluble GPVI (sGPVI) and standard markers of platelet activation has received little attention, such analysis may help reveal pathways mediating release of sCD147. We investigated the relationship between sCD147 and platelet markers including sGPVI, soluble and platelet-bound CD62P (P-selectin), active αIIbβ3 (assessed by PAC-1 binding) and platelet CD147 in 25 patients with stable angina pectoris (SAP), 13 patients with no coronary artery disease (CAD) and 10 healthy donors. Plasma levels of sCD147 significantly correlated with sGPVI (r = 0.46, p = .004), but did not correlate with any other platelet markers examined. Linear regression analysis identified that sCD147 levels could be predicted by sGPVI levels (β = .445, p = 0.003) and age (β = 0.304, p = 0.038), but were independent of potential clinical confounders such as CAD, diabetes and medication usage. As sCD147 strongly correlates with platelet-specific sGPVI, a common platelet source and/or mechanism of release may contribute to sCD147 levels in vivo. | |
| Pennings GJ et al. Platelets. 2013 Nov 18. [Epub ahead of print] | |
EMMPRIN expression positively correlates with WHO grades of astrocytomas and meningiomas |
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| High-grade primary brain tumors possessed poor outcome due to invasiveness. Extracellular matrix metalloproteinase inducer (EMMPRIN) stimulates peri-tumoral fibroblasts to secrete matrix metalloproteinase and promote invasiveness. This study hypothesized that high-grade brain tumors overexpress EMMPRIN. Analyzing the public delinked database from the Gene Expression Omnibus profile, the results showed that the EMMPRINmRNA level was higher in WHO grade IV (n = 81) than in grade III (n = 19, p < 0.0005) astrocytomas and non-tumor brain tissue controls (n = 23, p < 0.00001). The results of tissue microarray-based immunohistochemical (IHC) staining revealed that EMMPRIN levels positively correlated with WHO grades for astrocytomas (p = 0.008) and meningiomas (p = 0.048). EMMPRIN mRNA levels in conventional glioma cell lines (n = 36) was not less than those in glioma primary culture cells (n = 27) and glioblastoma stem-like cells (n = 12). The GBM8401, U87MG, and LN229 human glioma cell lines also overexpressed EMMPRIN. Hematoxylin and eosin, IHC, and immunofluorescence staining of xenografts confirmed that high-grade brain tumors overexpressed EMMPRIN. Lastly, Kaplan-Meier analysis revealed poorer survival in WHO grade IV (n = 56) than in grade III astrocytomas (n = 21, by log-rank test; p = 0.0001, 95 % CI: 1.842-3.053). However, in high-grade astrocytomas, there was no difference in survival between high and low EMMPRIN mRNA levels. Thus, this study identified that high-grade brain tumors overexpress EMMPRIN, which positively correlates with WHO grades in human astrocytomas and meningiomas, and suggests that EMMPRIN may be a therapeutic target of brain tumor. | |
| Tsai WC, et al. J Neurooncol. 2013 Sep;114(3):281-90. doi: 10.1007/s11060-013-1184-5. Epub 2013 Jul 2. | |
Intracoronary upregulation of platelet extracellular matrix metalloproteinase inducer (CD147) in coronary disease |
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| BACKGROUND:
CD147, also known as extracellular matrix metalloproteinase inducer, is present on circulating platelets and leukocytes in patients with coronary disease and is implicated in atherogenesis, and plaque rupture. We investigated whether CD147 (platelet, leukocyte and soluble) is upregulated within the coronary circulation in patients with stable coronary disease, and whether CD147 levels are associated with coronary shear stress levels. METHODS:A total of 25 patients undergoing intervention of a single coronary lesion had blood sampled within the coronary (n=15) and peripheral circulation (n=10). Platelet and leukocyte CD147 expression was measured by flow cytometry. Soluble CD147 was measured by enzyme-linked immunosorbent assays. Shear stress was calculated using computational fluid dynamics analysis. The effect of shear on platelet CD147 expression in vitro was investigated using a cone-plate viscometer. RESULTS: Platelet CD147 was higher in the coronary sinus (CS) compared to femoral vein (mean ± SD fluorescence intensity: 3.1 ± 0.7 vs. 2.2 ± 0.5, p=0.01). There was a significant linear trend for increased platelet CD147 expression from the proximal artery to the distal artery, and subsequently to the CS (p=0.01), indicating trans-lesion and transmyocardial upregulation. There were no differences between the various sites for monocyte, granulocyte or soluble CD147 levels (all p=ns). Trans-lesion gradients of CD147 did not correlate with shear stress (all p=ns). Blood subjected to shear in vitro had higher levels of platelet P-selectin (p=0.04) but similar levels of platelet CD147 (p=0.46) compared to rested blood. CONCLUSION: Platelet CD147 expression is upregulated in the coronary circulation in patients with stable coronary disease, but its upregulation is independent of shear stress. |
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| Yong A et al. Int J Cardiol. 2013 Jul 1;166(3):716-21. | |
Extracellular matrix metalloproteinase inducer (CD147) is a novel receptor on platelets, activates platelets, and augments nuclear factor kappaB-dependent inflammation in monocytes |
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| In atherosclerosis, circulating platelets interact with endothelial cells and monocytes, leading to cell activation and enhanced recruitment of leukocytes into the vascular wall. The invasion of monocytes is accompanied by overexpression of matrix metalloproteinases (MMPs), which are thought to promote atherosclerosis and trigger plaque rupture. Following interaction with itself, the extracellular matrix metalloproteinase inducer (EMMPRIN) induces MMP synthesis via a little-known intracellular pathway. Recently, we showed upregulation of EMMPRIN on monocytes during acute myocardial infarction. EMMPRIN also stimulates secretion of MMP-9 by monocytes and of MMP-2 by smooth muscle cells, indicating that it may be an important regulator of MMP activity. Expression of EMMPRIN on platelets has not been described until now. Here, we demonstrate that resting platelets show low surface expression of EMMPRIN, which is upregulated by various platelet stimulators (flow cytometry). EMMPRIN is located in the open canalicular system and in alpha granules of platelets (according to electron microscopy and sucrose gradient ultracentrifugation). Platelet stimulation with recombinant EMMPRIN-Fc induced surface expression of CD40L and P-selectin (according to flow cytometry), suggesting that EMMPRIN-EMMPRIN interaction activates platelets. Coincubation of platelets with monocytes induced EMMPRIN-mediated nuclear factor kappaB activation (according to Western blot) in monocytes with increased MMP-9 (zymography), interleukin-6, and tumor necrosis factor-alpha secretion (according to ELISA) by monocytes. In conclusion, EMMPRIN displays a new platelet receptor that is upregulated on activated platelets. Binding of EMMPRIN to platelets fosters platelet degranulation. Platelet-monocyte interactions via EMMPRIN stimulate nuclear factor kappaB-driven inflammatory pathways in monocytes, such as MMP and cytokine induction. Thus, EMMPRIN may represent a novel target to diminish the burden of protease activity and inflammation in atherosclerosis. | |
| Schmidt R et al. Circ Res. 2008 Feb 15;102(3):302-9. Epub 2007 Nov 29. | |
EMMPRIN promotes angiogenesis, proliferation, invasion and resistance to sunitinib in renal cell carcinoma, and its level predicts patient outcome |
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| PURPOSE:
Extracellular matrix metalloproteinase inducer (EMMPRIN) has been reported to play crucial roles, including in angiogenesis, in several carcinomas. However, the correlation between EMMPRIN levels and angiogenesis expression profile has not been reported, and the role of EMMPRINin renal cell carcinoma (RCC) is unclear. In the present study, we evaluated the association of EMMPRIN with angiogenesis, its value in prognosis, and its roles in RCC. EXPERIMENTAL DESIGN: EMMPRIN expression was examined in 50 RCC patients treated with radical nephrectomy. Angiogenesis, proliferation, and invasion activity were evaluated using EMMPRIN knockdown RCC cell lines. The size of EMMPRIN-overexpressing xenografts was measured and the degree of angiogenesis was quantified. EMMPRIN expression was evaluated in RCC patients who received sunitinib therapy and in sunitinib-resistant cells. Further, the relation between EMMPRIN expression and sensitivity to sunitinib was examined. RESULTS: EMMPRIN score was significantly associated with clinicopathological parameters in RCC patients, as well as being significantly correlated with microvessel area (MVA) in immature vessels and with prognosis. Down-regulation of EMMPRIN by siRNA led to decreased VEGF and bFGF expression, cell proliferation, and invasive potential. EMMPRIN over-expressing xenografts showed accelerated growth and MVA of immature vessels. EMMPRIN expression was significantly increased in patients who received sunitinib therapy as well as in sunitinib-resistant 786-O cells (786-suni). EMMPRIN-overexpressing RCC cells were resistant to sunitinib. CONCLUSION:Our findings indicate that high expression of EMMPRIN in RCC plays important roles in tumor progression and sunitinib resistance. Therefore, EMMPRIN could be a novel target for the treatment of RCC. |
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| Sato M, et al.PLoS One. 2013 Sep 20;8(9):e74313. doi: 10.1371/journal.pone.0074313. | |
Extracellular vesicles secreted from cancer cell lines stimulate secretion of MMP-9, IL-6, TGF-β1 and EMMPRIN |
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| Extracellular vesicles (EVs) are key contributors to cancer where they play an integral role in cell-cell communication and transfer pro-oncogenic molecules to recipient cells thereby conferring a cancerous phenotype. Here, we purified EVs using straightforward biochemical approaches from multiple cancer cell lines and subsequently characterized these EVs via multiple biochemical and biophysical methods. In addition, we used fluorescence microscopy to directly show internalization of EVs into the recipient cells within a few minutes upon addition of EVs to recipient cells. We confirmed that the transmembrane protein EMMPRIN, postulated to be a marker of EVs, was indeed secreted from all cell lines studied here. We evaluated the response to EV stimulation in several different types of recipient cells lines and measured the ability of these purified EVs to induce secretion of several factors highly upregulated in human cancers. Our data indicate that purified EVs preferentially stimulate secretion of several proteins implicated in driving cancer in monocytic cells but only harbor limited activity in epithelial cells. Specifically, we show that EVs are potent stimulators of MMP-9, IL-6, TGF-β1 and induce the secretion of extracellular EMMPRIN, which all play a role in driving immune evasion, invasion and inflammation in the tumor microenvironment. Thus, by using a comprehensive approach that includes biochemical, biological, and spectroscopic methods, we have begun to elucidate the stimulatory roles. | |
| Redzic JS, et al. PLoS One. 2013 Aug 1;8(8):e71225. doi: 10.1371/journal.pone.0071225. Print 2013. | |
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| CD147 (Soluble) (Human) ELISA Kit Code No.: SK00678-01 Size: 96 T Price: $420.00 USD Standard range:6.25-400 pg/ml Sensitivity: 3 pg/ml Sample type: plasma, serum Intra-CV: 4-6% Inter-CV: 8-10% Data Sheet: PDF |
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| Name | Code |
Size |
Price ($) |
| CD147 (Soluble) (Human) ELISA Kit | 96 T |
420.00 |
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| Cd147 (Soluble) (Human), Standard for SK00678-01 | 678-01-02 |
0.4 ng |
80.00 |
| Anti CD147 (Human) IgG HRP | 678-01-03 |
96 xrns |
160.00 |
| Soluble CD147 (EMMPRIN) (Human) Rec. | 00678-02-10 |
10 ug |
120.00 |
| Soluble CD147 (EMMPRIN) (Human) Rec. | 10 ug |
310.00 |
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| Soluble CD147 (EMMPRIN) (Human) Rec. | 00678-03-100 |
100 ug |
460.00 |
| Soluble CD147 (EMMPRIN) (Human) Rec. | 00678-03-1000 |
1 mg |
Inquire |
| Soluble CD147 (EMMPRIN) (Human) Fc Tag | 00678-04-100 |
100 ug |
420.00 |
| Soluble CD147 (EMMPRIN) (Human) Fc Tag | 00678-04-1000 |
1 mg |
Inquire |
| Anti Soluble CS147 (EMMPRIN) (Human) IgG (WB, E) | 50 ug |
260.00 |
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| Anti Soluble CS147 (EMMPRIN) (Human) monoclonal Antibody (IHC) | A00678-04-50 |
50 ug |
260.00 |