Expression of CD147 on phorbol-12-myris-tate-13-acetate (PMA)-treated U937 cells differentiating into foam cells

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

“…28 Yue.et al demonstrated lipid loading reduced mCD147 expression but induced the generation of sCD147 in U937-derived foam cells and the secretion and activation of MMP-2 and MMP-9. 14 Tang, Y.et al demonstrated sCD147 may serve as its own counter-receptor and induce the expression of CD147 and the activity of MMPs through a positive feedback mechanism in fibroblast cells. 29 These studies both found the up-regulation of sCD147 was accompanied by a reduction of membrane-bound CD147(mCD147), thus suggested sCD147 may cleave from cell-surface and MMPs maybe involved in shedding.…”

“…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.…”

Plasma EMMPRIN levels in acute myocardial infarction and stable coronary artery disease

“…It is clear from the above-mentioned animal and human studies that there is a discrepancy in the relationship of soluble [11,33] and cell-associated [2,3,10,[30][31][32][33] EMMPRIN with stable CAD. This phenomenon is probably due to the protein not naturally being found in adequate amounts in peripheral circulation, or possibly at least partially due to use of the drugs that can affect plasma levels of EMMPRIN in this population.…”

“…Multiple logistic regression analysis for adjustment of possible confounders on the association between EMMPRIN and AMI. A number of animal or in vitro human studies suggested that EMMPRIN performs an important function both in the development of atheroma and in its rupture; for instance, it has been demonstrated that pro-atherogenic stimuli, such as low-density lipoproteins, CRP, advanced glycation end-products, and high glucose levels, can stimulate EMMPRIN expression in inflammatory cells [30][31][32], whose activity is among the major determinants of the vulnerability of an atheroma to rupture [14]. It has also been shown that EMMPRIN can initiate the activation of nuclear factor κB, which is involved in the inflammatory and proliferative responses of cells linking to atherogenesis [2,3].…”

Function of CD147 in Atherosclerosis and Atherothrombosis

“…In vitro data show that pro-atherogenic stimuli, such as low -density lipoproteins (LDLs), C-reaction protein (CRP), advanced glycation end-products, and high glucose levels, can stimulate CD147 expression in inflammatory cells [37–39]. Anti-atherogenic drugs, such as fluvastatin can inhibit CD147 expression in macrophages [39].…”