How Far Since Ellis?

Mallick, N. P.; Short, Colin D.; Hunt, Linda

doi:10.1159/000184325

Cited by 39 publications

(5 citation statements)

References 13 publications

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“…Clinical nephrologists recognize the important correlation between the degree of proteinuria and risk of progression of many types of renal disease [1][2][3]. As such, it is widely observed that patients with significant proteinuria are substantially more likely to develop end-stage renal failure than those without proteinuria.…”

Section: Introductionmentioning

confidence: 99%

Albumin stimulates p44/p42 extracellular-signal-regulated mitogen-activated protein kinase in opossum kidney proximal tubular cells

Dixon

Brunskill

2000

Clinical Science

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The presence of protein in the urine of patients with renal disease is an adverse prognostic feature. It has therefore been suggested that proteinuria per se may be responsible for the development of renal tubulo-interstitial scarring and fibrosis, and disturbances in tubular cell growth and proliferation. We have used the opossum kidney proximal tubular cell line to investigate the effects of albumin on cell growth. The effect of albumin on cell proliferation was investigated by cell counting and measurement of [(3)H]thymidine incorporation. We studied the effect of recombinant human albumin on the activity of p44/p42 extracellular-signal-regulated mitogen-activated protein kinase (MAP kinase ) using an in vitro kinase assay, and immunoblotting with antibodies against active extracellular-signal-regulated kinase (ERK). The effects of the ERK inhibitor PD98059 were also examined. Recombinant human albumin was found to stimulate proliferation of opossum kidney cells in a dose-dependent manner, with maximal stimulation at a concentration of 1 mg/ml. In addition, recombinant human albumin activated ERK in a time-dependent (maximal after 5 min) and dose-dependent (maximal at 1 mg/ml) fashion. These effects on cell proliferation and ERK activity were inhibited by PD98059, and were not reproduced by ovalbumin or mannitol. The data therefore indicate that albumin is able to stimulate growth and proliferation of proximal tubular cells that is dependent on the ERK family of MAP kinases. The potential importance of this pathway in the development of renal disease is discussed.

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Section: Introductionmentioning

confidence: 99%

Albumin stimulates p44/p42 extracellular-signal-regulated mitogen-activated protein kinase in opossum kidney proximal tubular cells

Dixon

Brunskill

2000

Clinical Science

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“…nuclear factor-B; tubulointerstitial damage THE IMPORTANT CORRELATION between the degree of proteinuria and the risk of progression of renal disease has been recognized (5,18). It is widely observed that patients with significant proteinuria are more likely to develop end-stage renal failure than those without proteinuria (21,23,25).…”

mentioning

confidence: 99%

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

Takaya

Koya

Isono

et al. 2003

American Journal of Physiology-Renal Physiology

113

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Persistent proteinuria has been indicated to be a major risk factor for the development of tubulointerstitial damage through a process of proinflammatory molecule expression. Monocyte chemoattractant protein-1 (MCP-1) was shown to contribute to recruitment of immune cells into the renal interstitium in acute and chronic renal diseases. However, the molecular mechanisms by which proteinuria causes MCP-1 expression in proximal tubular cells have not been fully clarified. In this study, we examined whether albumin overload-induced MCP-1 expression was regulated by mitogen-activated protein kinase (MAPK) in mouse proximal tubular (mProx) cells. Exposure of mProx cells to delipidated bovine serum albumin (BSA) induced mRNA and protein expression of MCP-1 in a time- and dose-dependent manner. BSA activated extracellular signal-regulated kinase (ERK1/2) and p38 MAPK. The MEK inhibitor U-0126 partially suppressed BSA-induced MCP-1 expression and MCP-1 promoter/luciferase reporter activity. U-0126 also inhibited an increase in nuclear factor-kappaB and activator protein-1 DNA-binding activity of MCP-1 promoter by protein overload in mProx cells. In addition, we found that U-0126 inhibited BSA-induced nuclear factor-kappaB reporter activity and inhibitory protein degradation in mProx cells. In conclusion, these findings indicate that ERK signaling is involved in BSA-induced MCP-1 expression in mProx cells.

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“…Reichert LJM, Koene RAP, Wetzels JFM: Urinary IgG excretion patients with proteinuria will retain normal renal funcas a prognostic factor in idiopathic membranous nephropathy. Clin tion for more than five years[41]. Proteinuria in itselfNephrol 48:79-84, 1997 10.…”

mentioning

confidence: 99%

Familial nephropathy differing from minimal change nephropathy and focal glomerulosclerosis

Branten

Born

Jansen

et al. 2001

Kidney International

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How Far Since Ellis?

Cited by 39 publications

References 13 publications

Albumin stimulates p44/p42 extracellular-signal-regulated mitogen-activated protein kinase in opossum kidney proximal tubular cells

Albumin stimulates p44/p42 extracellular-signal-regulated mitogen-activated protein kinase in opossum kidney proximal tubular cells

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

Familial nephropathy differing from minimal change nephropathy and focal glomerulosclerosis

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