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CCL2 — TLR4

Text-mined interactions from Literome

Kato et al., J Am Soc Nephrol 2004 (Peritonitis) : A prominent induction of monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein (MIP)-2 by MPMC was detected after lipid A stimulation and was strictly dependent on TLR4
Kurt-Jones et al., J Endotoxin Res 2004 : MEFs were highly responsive to TLR-ligand activation and secreted high levels of both IL-6 and MCP-1 in response to TLR ligands
Gutiérrez-Cañas et al., Rheumatology (Oxford) 2006 (Arthritis, Rheumatoid...) : The effects of VIP on basal or TNF-alpha or lipopolysaccharide (LPS) induced TLR2, TLR4 and MyD88 expression and its effects on TLR4 mediated CCL2 and CXCL8 chemokine production were studied by reverse transcription-polymerase chain reaction, western blotting and enzyme linked immunosorbent assay ... VIP treatment decreased CCL2 and CXCL8 chemokine production in response to TLR4 activation with LPS in RA FLS
Riccioli et al., J Immunol 2006 : Moreover, we studied the role of NF-kappaB and of MAPKs in regulating TLR mediated MCP-1 secretion by using inhibitors specific for each transduction pathway and we demonstrated a pivotal role of the IkappaB/NF-kappaB and JNK systems
Yoshimura et al., J Immunol 2007 : IFN-gamma mediated survival enables human neutrophils to produce MCP-1/CCL2 in response to activation by TLR ligands
Lee et al., Cell Signal 2008 : This study highlights the importance of cytosolic phospholipase A2 (cPLA2) mediated reactive oxygen species ( ROS ) signaling processes in the regulation of MCP-1 release as a result of toll-like receptor ( TLR ) activation
Masamune et al., J Gastroenterol 2008 : TLR ligands induced expression of monocyte chemoattractant protein 1 , cytokine induced neutrophil chemoattractant 1 ( a rat homolog of interleukin-8 ), and inducible nitric oxide synthase, but not proliferation or type I collagen production
Lee et al., Cell Microbiol 2009 : In addition, TLR2 , Dectin-1 and, to an extent, TLR4 are essential for the MU-mediated expression of CXCL8, CCL2 and LL-37 in keratinocytes
Ishikado et al., Atherosclerosis 2009 (Inflammation) : Soy phosphatidylcholine inhibited TLR4 mediated MCP-1 expression in vascular cells
Jia et al., J Immunol 2009 (Listeriosis) : The first phase is rapid, induces low-level production of MCP-1 , and is dependent on TLR/MyD88 signaling
Yeop Han et al., Diabetes 2010 (Hypertrophy...) : Silencing toll-like receptor-4 (TLR4) markedly reduced SAA and MCP-1 expression in response to palmitate but not glucose
Dasu et al., Am J Physiol Endocrinol Metab 2011 (Diabetes Mellitus, Type 2...) : Silencing TLR2, TLR4 , and p47phox with small inhibitory RNAs ( siRNAs ) significantly reduced superoxide release, NF-?B activity, IL-1ß, and MCP-1 secretion in HG and palmitate treated THP-1 cells
Agarwal et al., Arthritis Res Ther 2011 (Fibrosis...) : The ability of IFNa2 to regulate TLR induced interleukin (IL)-6 and CC chemokine ligand 2 production was also assessed
Tang et al., Contrib Nephrol 2011 (Diabetic Nephropathies...) : In human DN biopsies and PTEC, TLR4is upregulated and plays a permissive role in HG-induced IL-6 and CCL-2 overexpression and monocyte transmigration
Lin et al., J Am Soc Nephrol 2012 (Diabetes Mellitus, Experimental...) : Silencing of TLR4 with small interfering RNA attenuated high glucose induced I?B/NF-?B activation, inhibited the downstream synthesis of IL-6 and CCL-2 , and impaired the ability of conditioned media from high glucose treated proximal tubule cells to induce transmigration of mononuclear cells
Miura et al., Am J Physiol Gastrointest Liver Physiol 2012 (Fatty Liver...) : Toll-like receptor (TLR)4 ( -/- ), TLR9 ( -/- ), and MyD88 ( -/- ) mice had reduced hepatic macrophage infiltration with decreased MCP-1 and CCR2 expression because TLR signaling is a potent inducer of MCP-1
Salagianni et al., Circulation 2012 (Carotid Artery Diseases...) : Mechanistically, TLR7 interfered with macrophage proinflammatory responses to TLR2 and TLR4 ligands, reduced monocyte chemoattractant protein-1 production, and prevented expansion of Ly6C ( hi ) inflammatory monocytes and accumulation of inflammatory M1 macrophages into developing atherosclerotic lesions
Brancato et al., Wound Repair Regen 2013 (Disease Progression...) : The accumulation of CCL2 , CX3CL1, tumor necrosis factor-a, interleukin (IL)-6, IL-10, IL-12, and interferon-? in wound fluids was not TLR4 dependent