INT73047
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
However, the AA-induced activity of MMP-9 did not diminish in the presence of n-3 fatty acids, although the cellular fatty acid content revealed an ample availability of n-3 fatty acids after incubation. | |||||||||||||||
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As shown in Fig. 2B, MMP-9 activity was augmented already after 1 h incubation with AA and increased for at least 6 h. | |||||||||||||||
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Activated MMP1, MMP3 and latent forms of MMP2 and MMP9 are regulated and inhibited by endogenous proteins known as tissue inhibitors of metalloproteinase TIMP1 and TIMP2 [17]. | |||||||||||||||
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1 mRNA were upregulated at POD 5, then NAMPT, EGR1 and MMP9 mRNA. | |||||||||||||||
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Experiments where MonoMac 6 cells were pre exposed to AA for increasing periods of time (Fig. 2B) showed that the system delivering MMP-9 to the medium was activated already after 1 h incubation and increased for at least 6 h. | |||||||||||||||
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As shown in Fig 5, Ly 294002 blocked the induction of MMP-9 by AA and PMA in a dose-dependent manner. | |||||||||||||||
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The transcriptional regulatory mechanism was confirmed by the increase of MMP-9 mRNA by AA treatment. | |||||||||||||||
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It is not known whether AA causes degranulation in MonoMac 6 cells, but the continued accumulation of MMP-9 in the incubation medium speaks for additional mechanisms. | |||||||||||||||
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Published results thus suggest that localized increase in MMP-9 associated with an inflammatory process in the vascular wall has the potential to weaken the tissue structure thus increasing the risk for plaque rupture. | |||||||||||||||
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These results suggest that the surface expression of CD44 is required for the activation of MMP-9. | |||||||||||||||
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This implies that CRP and MMP-9, at least to some extent, could be markers of different physiological pathways. | |||||||||||||||
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As shown in Fig. 2B, MMP-9 activity was augmented already after 1 h incubation with AA and increased for at least 6 h. | |||||||||||||||
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Elevated levels of circulating matrix metalloproteinase-9 (MMP-9) have been demonstrated in patients with established coronary artery disease (CAD). | |||||||||||||||
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So far, most studies exploring elevated levels of MMP-9 and its association to coronary artery disease (CAD) have been based on a experimental or clinical design, the latter showing elevated levels of plasma MMP-9 in patients with CAD [13][18]. | |||||||||||||||
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Elevated levels of circulating matrix metalloproteinase-9 (MMP-9) have been demonstrated in patients with established coronary artery disease (CAD). | |||||||||||||||
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RESULTS: A correlation was found between the increasing levels of matrix metalloproteinases 2 and 9 and the grade of degenerative disc disease. | |||||||||||||||
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MMP-9 activity is controlled at different levels: transcriptional activation of the gene by cytokines and other factors, activation of the pro-enzyme by various enzymes like serine proteases and regulation by specific tissue inhibitors of the matrix metalloproteinases (TIMPs). | |||||||||||||||
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Since there was an increase in MMP-9 activity in the conditioned media of PC3/OPN cells (Figure 1B), we determine the surface levels of MMP-9 in PC3 cell lines (Figure 2C). | |||||||||||||||
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MMP-9 activity was greatly enhanced in OPN over expressing clones which are represented as C1C4 (B, lanes 36) as compared with PC3 cells (lane 2). | |||||||||||||||
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Metalloproteinases (MMP-2 and MMP-9) are upregulated in the optic nerve head of glaucoma patients. | |||||||||||||||
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General Comments
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