High glucose induces MCP-1 expression partly via tyrosine kinase–AP-1 pathway in peritoneal mesothelial cells

Lee, Sang Koo; Kim, Byung Sik; Yang, Woo Jin; Kim, Soon Bae; Park, Su Kil; Park, Jung Sik

doi:10.1046/j.1523-1755.2001.00770.x

Cited by 46 publications

(41 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inflammatory cytokines and growth factors, such as platelet-derived growth factor (PDGF) and interleukin-1, can trigger the expression of MCP-1 through activation of several signalling pathways such as extracellular signal-related kinase (ERK)1/2 [2], p38 mitogen-activated protein (MAP) kinase [3], protein kinase C [4], activator protein (AP)-1 [5] and nuclear factor (NF)-kB [6]. We have reported that integrin-mediated activation of intracellular signalling molecules also induces MCP-1 expression in mesangial cells [7], suggesting that abnormal remodelling of ECM observed in many types of glomerular diseases can upregulate MCP-1 expression.…”

Section: Introductionmentioning

confidence: 99%

Synergistic induction of monocyte chemoattractant protein-1 by integrins and platelet-derived growth factor via focal adhesion kinase in mesangial cells

Kanegae¹,

Tamura²,

Kabashima³

et al. 2005

Nephrology Dialysis Transplantation

View full text Add to dashboard Cite

Background. Growth factors, extracellular matrix and its receptor integrins are upregulated in various glomerular diseases. We investigated the mechanism of collaboration between integrins and plateletderived growth factor (PDGF) in focal adhesion kinase (FAK)-and extracellular signal-related kinase (ERK)1/2-mediated signal pathways that lead to monocyte chemoattractant protein (MCP)-1 expression in cultured rat mesangial cells (MCs). Methods. Serum-starved MCs were plated on fibronectin-or polylysine-coated plates with or without PDGF, and examined for phosphorylation of ERK1/2, mitogen-activated protein or ERK kinase (MEK)1/2 and FAK by western blotting, and for expression of MCP-1 mRNA and protein by reverse transcriptionpolymerase chain reaction (RT-PCR) and enzymelinked immunosorbent assay (ELISA), respectively. The effects of dominant-negative FAK on MCP-1 expression were examined. Results. Cell adhesion to fibronectin increased phosphorylation of FAK, MEK1/2 and ERK1/2, and induced MCP-1 mRNA and protein expression. PDGF increased phosphorylation of FAK, MEK1/2 and ERK1/2 even without cell adhesion to fibronectin, and induced MCP-1 mRNA and protein expression. PDGF with integrin activation by fibronectin synergistically increased phosphorylation of FAK, MEK1/2 and ERK1/2, and expression of MCP-1 mRNA and protein. Dominant-negative FAK attenuated fibronectin enhancement of PDGF-induced ERK1/2 phosphorylation and MCP-1 expression, indicating involvement of FAK in this signalling. Conclusions.Our results suggest the cooperative role of integrin and PDGF receptor in activation of the ERK pathway possibly via FAK in MCs. The synergistic activation of integrin and PDGF signalling may play an important role in the progression of glomerular diseases through the induction of MCP-1.

show abstract

Section: Introductionmentioning

confidence: 99%

Synergistic induction of monocyte chemoattractant protein-1 by integrins and platelet-derived growth factor via focal adhesion kinase in mesangial cells

Kanegae¹,

Tamura²,

Kabashima³

et al. 2005

Nephrology Dialysis Transplantation

View full text Add to dashboard Cite

show abstract

“…We previously demonstrated that fish oil reduces NF-B activation, inflammation, and renal damage in a salt-sensitive model of hypertension, an effect that is only in part due to reduction in blood pressure (16). A number of in vitro studies implicated activation of ERK, NF-B, and/or AP-1 in the transcriptional regulation of MCP-1 in response to a variety of proinflammatory cytokines (38,43,46,47,52,73,79).…”

mentioning

confidence: 99%

n-3 Fatty acids block TNF-α-stimulated MCP-1 expression in rat mesangial cells

Díaz-Encarnación¹,

Warner²,

Cheng³

et al. 2011

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…In addition to renal fibrosis, MCP1 is also implicated in the pathogenesis of peritoneal fibrosis. In peritoneal fibrosis, it has been suggested that high glucose concentration in conventional peritoneal dialysis solutions, which are used for continuous ambulatory peritoneal dialysis, plays a role in fibrotic lesions by increasing MCP1 gene expression (5,6).…”

mentioning

confidence: 99%

Hypertonicity-Induced Expression of Monocyte Chemoattractant Protein-1 through a Novel Cis-Acting Element and MAPK Signaling Pathways

Kojima

Taniguchi

Tsuzuki

et al. 2010

The Journal of Immunology

View full text Add to dashboard Cite

MCP1 is upregulated by various stimuli, including LPS, high glucose, and hyperosmolality. However, the molecular mechanisms of transcriptional regulation of the MCP1 gene under hyperosmolar conditions are poorly understood. Treatment of NRK52E cells with NaCl or mannitol resulted in significant elevation of MCP1 mRNA and protein in a time- and dose-dependent manner. Treatment with a p38MAPK inhibitor (SB203580), an ERK inhibitor (PD98059), or an MEK inhibitor (U0126), suppressed the increase in MCP1 expression caused by hypertonic NaCl, whereas a JNK inhibitor (SP600125) and an AP1 inhibitor (curcumin) failed to attenuate MCP1 mRNA expression by NaCl. In the 5′-flanking region of the MCP1 gene, there is a sequence motif similar to the consensus TonE/ORE as well as the consensus C/E binding protein (BP), NF-κB, and AP1/Sp1 sites. Luciferase activity in cells transfected with reporter constructs containing a putative TonE/ORE element (MCP1-TonE/ORE) enhanced reporter gene expression under hypertonic stress. Results of electrophoretic gel mobility shift assay showed a slow migration of the MCP1-TonE/ORE probe, representing the binding of TonEBP/OREBP/NFAT5 to this enhancer element. These results indicate that the 5′-flanking region of MCP1 contains a hypertonicity-sensitive cis-acting element, MCP1-TonE/ORE, as a novel element in the MCP1 gene. Furthermore, p38MAPK and MEK–ERK pathways appear to be, at least in part, involved in hypertonic stress-mediated regulation of MCP1 expression through the MCP1-TonE/ORE.

show abstract

High glucose induces MCP-1 expression partly via tyrosine kinase–AP-1 pathway in peritoneal mesothelial cells

Abstract: : High glucose induced mesothelial MCP-1 expression partly via the tyrosine kinase-AP-1 pathway.

Cited by 46 publications

References 36 publications

Synergistic induction of monocyte chemoattractant protein-1 by integrins and platelet-derived growth factor via focal adhesion kinase in mesangial cells

Synergistic induction of monocyte chemoattractant protein-1 by integrins and platelet-derived growth factor via focal adhesion kinase in mesangial cells

n-3 Fatty acids block TNF-α-stimulated MCP-1 expression in rat mesangial cells

Hypertonicity-Induced Expression of Monocyte Chemoattractant Protein-1 through a Novel Cis-Acting Element and MAPK Signaling Pathways

Contact Info

Product

Resources

About