Involvement of ERK pathway in albumin-induced MCP-1 expression in mouse proximal tubular cells

Takaya, Kiho; Koya, Daisuke; Isono, Motohide; Sugimoto, Toshiro; Sugaya, Takeshi; Kashiwagi, Atsunori; Haneda, Masakazu

doi:10.1152/ajprenal.00230.2002

Cited by 113 publications

(101 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MCP-1 production has been reported in tubular epithelial cells in unilateral ureter obstruction model 52 and cultured renal proximal tubular epithelial cells. 53 We also found MCP-1 production in tubular epithelial cells by immunohistochemistry that was decreased in PAFR-KO mice. Furthermore, PAF activates nuclear factor-B, 54 which is critical for production of MCP-1 in tubular epithelial cells.…”

Section: Discussionsupporting

confidence: 54%

Attenuation of Folic Acid-Induced Renal Inflammatory Injury in Platelet-Activating Factor Receptor-Deficient Mice

Doi

Okamoto

Negishi

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

Platelet-activating factor (PAF), a potent lipid mediator with various biological activities, plays an important role in inflammation by recruiting leukocytes. In this study we used platelet-activating factor receptor (PAFR)-deficient mice to elucidate the role of PAF in inflammatory renal injury induced by folic acid administration. PAFR-deficient mice showed significant amelioration of renal dysfunction and pathological findings such as acute tubular damage with neutrophil infiltration, lipid peroxidation observed with antibody to 4-hydroxy-2-hexenal (day 2), and interstitial fibrosis with macrophage infiltration associated with expression of monocyte chemoattractant protein-1 and tumor necrosis factor-␣ in the kidney (day 14). Acute tubular damage was attenuated by neutrophil depletion using a monoclonal antibody (RB6-8C5), demonstrating the contribution of neutrophils to acute phase injury. Macrophage infiltration was also decreased when treatment with a PAF antagonist (WEB2086) was started after acute phase. In vitro chemotaxis assay using a Boyden chamber demonstrated that PAF exhibits a strong chemotactic activity for macrophages. These results indicate that PAF is involved in pathogenesis of folic acid-induced renal injury by activating neutrophils in acute phase and macrophages in chronic interstitial fibrosis. Inhibiting the PAF pathway might be therapeutic to kidney injury from inflammatory cells.

show abstract

Section: Discussionsupporting

confidence: 54%

Attenuation of Folic Acid-Induced Renal Inflammatory Injury in Platelet-Activating Factor Receptor-Deficient Mice

Doi

Okamoto

Negishi

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…In contrast to ERK5, many of the genes up-regulated in response to ERK1/2 in these cells were observed previously in other systems, including FOS (42), HAS2 (43), PTHLH (44), BIRC3/AIP1 (45), CCL2/MCP1 (46,47), CXCL1 (48), CXCL2 (49), IL-6 (50), IL-8 (51), PTGS2 (52), and IL1B (53). No genes were found to be repressed by ERK1/2 signaling in RPE cells.…”

Section: Characterization Of Map Kinase Signaling In Rpe Cells-mi-supporting

confidence: 63%

Global Gene Expression Analysis of ERK5 and ERK1/2 Signaling Reveals a Role for HIF-1 in ERK5-mediated Responses

Schweppe

Cheung

Ahn

2006

Journal of Biological Chemistry

View full text Add to dashboard Cite

ERK5 is a recently characterized MAPK, which is most similar to the well studied ERK1/2 subfamily but uses distinct mechanisms to elicit responses. To understand the specificity of signaling through ERK5 versus ERK1/2, we examined global gene expression changes in response to each pathway. Microarray measurements in retinal pigment epithelial cells revealed 36 genes regulated by ERK5, all which were novel targets for this pathway. 39 genes were regulated by ERK1/2, which included 11 known genes. Of these genes, 19 were regulated by both pathways. Inspection of the 17 genes uniquely regulated by ERK5 revealed that 14 genes (82%) were previously associated with hypoxia via regulation by HIF-1. In contrast, 16 genes (84%) regulated by either ERK5 or ERK1/2 were implicated in hypoxia, most through mechanisms independent of HIF-1. Of the 20 genes regulated by ERK1/2, only 9 were implicated in hypoxia and were not well characterized hypoxia targets. Thus, unlike ERK5, a mechanistic link between ERK1/2 and HIF-1/HRE could not be established on the basis of gene regulation. Activation of both pathways enhanced transcription from a hypoxiaresponse element and increased HIF-1␣ protein expression. In contrast, ERK5 but not ERK1/2 elevated transcription through GAL4-HIF-1. Most interestingly, ERK5 is not significantly activated by hypoxia in retinal pigment epithelial cells, indicating that ERK5 regulation of these genes is relevant in normoxia rather than hypoxia. Thus, ERK5 and ERK1/2 differ in their mechanisms of gene regulation, and indicate that ERK5 may control hypoxia-responsive genes by a mechanism independent of HIF-1␣ expression control.

show abstract

“…A total of 2 ϫ 10 7 murine proximal tubular cell line (mProx; CLEA, Tokyo, Japan) 32,33 were plated in DMEM with 10% FCS, 25 g/ml penicillin, and streptomycin for 24 to 36 h to achieve 80 to 90% confluence. Cellular stress was assessed initially by serum starvation.…”

Section: In Vitro Assays With Murine Proximal Tubular Epithelial Cellsmentioning

confidence: 99%

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Suzuki¹,

Tanifuji²,

Akiba³

et al. 2008

Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

Proteinuria is a key factor in the progression of tubulointerstitial injury. Recently, tubular ischemia as a result of loss of peritubular capillaries has been identified as another major contributor to disease progression, but the relative contribution of these insults on tubulointerstitial damage is unknown. Anti-glomerular basement membrane glomerulonephritis was induced in wild-type (WT) and Fc receptor knockout (FcRKO) mice, which have been shown to be relatively protected against glomerular endothelial injury. Despite comparable degrees of proteinuria, WT mice developed significantly worse renal function than FcRKO mice, along with higher expression of both type I collagen and kidney injury molecule-1 (a sensitive marker of acute tubular injury) by real-time PCR and immunohistochemistry. In addition, compared with FcRKO mice, WT mice exhibited a greater decrease in peritubular red blood cell velocity by intravital videomicroscopy and a marked increase of tissue hypoxia. In vitro, kidney injury molecule-1 expression increased in cultured mouse proximal tubular epithelial cells in response to cellular stresses, including hypoxia, starvation, and exposure to excessive protein; therefore, it is suggested that hypoxic insults more strongly influence tubulointerstitial damage than proteinuria alone in models of subacute renal disease.

show abstract

Involvement of ERK pathway in albumin-induced MCP-1 expression in mouse proximal tubular cells

Cited by 113 publications

References 34 publications

Attenuation of Folic Acid-Induced Renal Inflammatory Injury in Platelet-Activating Factor Receptor-Deficient Mice

Attenuation of Folic Acid-Induced Renal Inflammatory Injury in Platelet-Activating Factor Receptor-Deficient Mice

Global Gene Expression Analysis of ERK5 and ERK1/2 Signaling Reveals a Role for HIF-1 in ERK5-mediated Responses

Peritubular Ischemia Contributes More to Tubular Damage than Proteinuria in Immune-Mediated Glomerulonephritis

Contact Info

Product

Resources

About