A uremic solute, P-cresol, inhibits the proliferation of endothelial progenitor cells via the p38 pathway

Circ J. 2011;75(9):2252-9. doi: 10.1253/circj.cj-11-0046. Epub 2011 Jul 12.

Abstract

Background: Endothelial dysfunction is a consistent finding in uremic patients. Whether the uremic solutes, p-cresol and indoxyl sulfate, affect the cellular function of endothelial progenitor cells (EPCs) was tested.

Methods and results: EPCs were isolated from healthy adults and treated with p-cresol (10-80 μg/ml) or indoxyl sulfate (25-200 μg/ml) with ranges of concentration similar to those found in uremic patients. The effect of p-cresol or indoxyl sulfate on the viability of EPCs was examined by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In vitro angiogenesis of EPCs was tested by a matrigel assay. Signal pathways activated by these solutes were also studied. The viability of EPCs was dose- and time- dependently inhibited by p-cresol and indoxyl sulfate, respectively (both P < 0.05). The angiogenesis capacity of EPCs was suppressed significantly by p-cresol but not by indoxyl sulfate. Phosphorylated p38 and Erk1/2 was increased by p-cresol, while P38 inhibitor SB203580 reversed the effect of p-cresol in the MTT assay. Notably, a dose of 80 μg/ml p-cresol decreased the Notch1 intracellular domain level in EPCs.

Conclusions: This study has demonstrated that p-cresol inhibits proliferation of EPCs via activation of p38 MAPK pathways. P-cresol also attenuates angiogenesis function of EPCs and interferes with the Notch1 path-way.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Cresols / chemistry
  • Cresols / pharmacology*
  • Endothelial Cells / cytology
  • Endothelial Cells / enzymology*
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Humans
  • Imidazoles / pharmacology
  • MAP Kinase Signaling System / drug effects*
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Neovascularization, Physiologic / drug effects
  • Phosphorylation / drug effects
  • Pyridines / pharmacology
  • Receptor, Notch1 / metabolism
  • Stem Cells / cytology
  • Stem Cells / enzymology*
  • Urine / chemistry*
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Cresols
  • Enzyme Inhibitors
  • Imidazoles
  • NOTCH1 protein, human
  • Pyridines
  • Receptor, Notch1
  • 4-cresol
  • MAPK1 protein, human
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • p38 Mitogen-Activated Protein Kinases
  • SB 203580