MMP-9 (matrix metalloproteinase-9), a marker of atherosclerosis previously reported to be associated with NADPH oxidase overactivity, was quantified by ELISA in plasma samples.
Matrix metallopeptidase-9 (MMP-9) was revealed to be a direct target gene of miR-133a-3p, which was upregulated in the blood and vascular plaque tissue of patients with AS.
Altogether, these findings suggest that Lcn2 deficiency promotes lesion growth in earlier stages of the disease while it decreases MMP-9 activity and necrotic core size in advanced atherosclerosis.
Based on the studies performed so far, it is assumed that IL-17 contributes to development of atherosclerosis by means of: stimulation of production of proinflammatory compounds; induction of apoptosis of endothelial cells and heart muscle cells; stimulation of von Willebrand factor production; and induction of the matrix metalloproteinase-9 (atherosclerotic plaque rupture).
Cholestin reduces TNF-α-stimulated MMP-2 and MMP-9 expression as well as downregulating NF-κB activation and intracellular ROS formation in HASMCs, supporting the notion that the natural compound Cholestin may have potential application in clinical atherosclerosis disease.
Herein we review the involvement of MMP-9 in a variety of autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, systemic sclerosis, rheumatoid arthritis, multiple sclerosis, polymyositis and atherosclerosis.
Herein, patients with atherosclerosis showed higher MMP9, a promising biomarker for atherosclerosis, and lower Bmal1 and Clock expression in the plasma.
However, the severity of atherosclerosis in coronary artery or in stent restenosis was not related to any polymorphism of stromelysin-1 or gelatinase B.
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.
In summary, MMP-9 mRNA expression is enhanced in monocytes from HD and CAPD patients, and the enhancement may be, in part, associated with cardiovascular complications, including atherosclerosis, in dialysis patients.
In the present study, we investigated the expression of matrix metalloproteinase-9 (MMP-9), which is one of key mediators of atherosclerosis progression, in oxLDL-treated human umbilical vein endothelial cells (HUVEC)-C cells.
In this study we tested the hypothesis that variation in the matrix metalloproteinase-9 gene influences the development of atherosclerosis.Three common polymorphisms, i.e.
Our results suggest that the expression of CD40 and CD40L in the blood cells and the activities of MMP-2 and MMP-9 in plasma were higher in As group than those in Normal group, indicating that they may contribute to the formation of atherosclerosis.
P2X7R may serve a crucial role in the development of atherosclerosis; therefore, the present study aimed to determine whether P2X7R regulated the expression of EMMPRIN and MMP‑9 in phorbol 12‑myristate 13‑acetate (PMA)‑induced macrophages.
Plasma MMP-9 levels were related neither to MMP-9 PM nor to plaque type, and were related to gender and extension of atherosclerosis in carotid arteries.