Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.23 (MMP)
 4,246 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, the gene expression patterns of peripheral blood leucocytes (PBL) from Japanese flounder Paralichthys olivaceus were analyzed during the course of monogenean parasite Neoheterobothrium hirame infection in order to select candidates for molecular biomarkers of infection. cDNA microarray analysis was performed to compare the gene expression patterns of PBL between infected and non-infected fishes. Among the 797 genes analyzed, 45 genes (5.6%) changed their expression levels. These genes included specific and non-specific immune-related genes (matrix metalloproteinase[MMP]-9, MMP-13, leukotriene B4 receptor, CD20 receptor, MHC [major histocompatibility complex] Class I, MHC Class II beta-chain, immunoglobulin light chain and immunoglobulin heavy chain). Significant up- and down-regulation of some unknown genes was also observed. Several candidates for infection-marker genes were selected for further study. These genes included MMP-9, MMP-13, leukotriene b4 receptor, CD20 receptor, immunoglobulin heavy chain, immunoglobulin light chain and unknown genes coded as B613, E25, LB3(8), WE2(3), WE8-18R and WF12-18R.
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PMID:Microarray analyses of gene expression in Japanese flounder Paralichthys olivaceus leucocytes during monogenean parasite Neoheterobothrium hirame infection. 1752 46

5-Lipoxygenase (5-LO) has been suggested as a modulator of atherosclerotic plaque instability, however, its role in MMP production in vascular smooth muscle cells (VSMC) is still unclear. Thus, this study investigated the role of 5-LO in HNE-enhanced MMP-2 production in VSMC, and the mechanisms by which this enzyme could be activated by HNE. VSMC stimulated with HNE (1 microM) produced MMP-2, which was markedly attenuated in 5-LO-deficient VSMC as well as in cells pretreated with a FLAP inhibitor, MK886, confirming a role for 5-LO metabolites in HNE-enhanced MMP-2 production. Related to these results, HNE increased nuclear translocation of 5-LO promoting 5-LO activity, which was attenuated not only by SB203580, a p38 MAPK inhibitor, but also by PD98059, an ERK inhibitor. In parallel, phosphorylation of p38 MAPK and ERK occurred as early as 15 min after exposure to HNE, suggesting a potential role for p38 MAPK and ERK pathways in HNE-induced activation of 5-LO. Among leukotriene (LT) receptor antagonists, U-75302, a BLT receptor antagonist, but not MK-571 and Rev-5901, cysLT receptor antagonists, showed an inhibitory effect on HNE-enhanced MMP-2 production. Moreover, MMP-2 production in VSMC was also significantly increased by LTB(4), but not by LTC(4) and LTD(4). Collectively, these data suggest that 5-LO mediates HNE-enhanced MMP-2 production via LTB(4)-BLT receptor pathways, consequently leading to atherosclerotic plaque instability.
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PMID:Participation of 5-lipoxygenase-derived LTB(4) in 4-hydroxynonenal-enhanced MMP-2 production in vascular smooth muscle cells. 1958 28