Gene interactions and pathways from curated databases and text-mining

◀ Back to MMP9

IL18 — MMP9

Text-mined interactions from Literome

Meisser et al., Mol Hum Reprod 1999 : The aim of this study was to determine the effects of tumour necrosis factor alpha (TNF), interleukin-1 alpha (IL-1alpha), macrophage colony stimulating factor ( MCSF ) and transforming growth factor beta ( TGFbeta ) on the secretion of matrix metalloproteinases ( MMP ) , human chorionic gonadotrophin ( HCG ) and fetal fibronectin ( fFN ) by purified first trimester cytotrophoblastic cells (CTB) in vitro
Quiding-Järbrink et al., Infect Immun 2001 (Tuberculosis) : In conclusion, we show that mycobacterial infection induces MMP-9 activity both in vitro and in vivo and that this is regulated by TNF-alpha, IL-18 , and IFN-gamma
Abraham et al., Int Immunol 2002 : The present study examined differential effects of pro-inflammatory [IL-18 , IL-12 and tumor necrosis factor (TNF)-alpha ] versus anti-inflammatory ( IL-4 ) cytokines on the modulation of MMP and their endogenous tissue inhibitors ( TIMP ) expression in the U937 cell line
Nold et al., Naunyn Schmiedebergs Arch Pharmacol 2003 : As biological activity of matrix metalloproteinase-9 (MMP-9) has been identified as a hallmark in the pathogenesis of these diseases, effects of IL-18 on MMP-9 production by human peripheral blood mononuclear cells ( PBMC ) were investigated ... Here we report that IL-18 augmented production of MMP-9 by PBMC ... IL-18 also induced secretion of MMP-9 from human whole blood cultures
Sun et al., Connect Tissue Res 2003 (Arthritis, Rheumatoid) : Furthermore, the induction of the MMP expression and activities by interleukin-1 was suppressed by the oscillatory shear
Zhang et al., Leuk Res 2004 (Leukemia, Myeloid...) : Moreover, IL-18 could significantly increase MMP-9 but not MMP-2 production at both mRNA and/or protein level, slightly up-regulate TIMP-1 mRNA, and clearly induce TIMP-2 mRNA secretion
Dai et al., Ann Rheum Dis 2005 (Arthritis...) : In chondrocytes responding to IL18, IL18 ( 1-100 ng/ml ) slightly increased the production of MMP-1, MMP-3 , and MMP-13, which was blocked by NF-kappaB inhibitor and p38 mitogen activated protein kinase inhibitor
Chandrasekar et al., J Biol Chem 2006 (Atherosclerosis) : Specific antisense or small interfering RNA reagents for these transcription factors reduced IL-18 mediated MMP9 transcription ... Together, our results indicate for the first time that the proatherogenic cytokine IL-18 induces human coronary artery SMC migration in an MMP9 dependent manner ... Because we demonstrated previously that the proinflammatory and proatherogenic cytokine interleukin-18 (IL-18) stimulates SMC proliferation ( Chandrasekar, B., Mummidi, S., Valente, A. J., Patel, D. N., Bailey, S. R., Freeman, G. L., Hatano, M., Tokuhisa, T., and Jensen, L. E. ( 2005 ) J. Biol. Chem. 280, 26263-26277 ), we investigated whether IL-18 induces SMC migration in an MMP dependent manner and whether the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor atorvastatin can inhibit this response
Giannelli et al., J Interferon Cytokine Res 2006 : In this study, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), commonly elevated in chronic C hepatitis, stimulate the production of matrix metalloprotease-9 (MMP-9) by human hepatocytes at a transcriptional and translational level, but the addition of recombinant interferon-alpha2b ( rIFN-alpha2b ) hampers this effect
Alexander et al., Curr Eye Res 1998 : A phorbol mitogen ( TPA ), and TNF alpha and beta, interleukin-1 alpha and PDGF BB stimulate gelatinase B , stromelysin, interstitial collagenase and TIMP-1 expression, while having negligible effects on gelatinase A expression ; TIMP-2 levels are reduced by TNF but not affected by the other treatments