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Extracellular ATP augments mesangial cell growth induced by multiple growth factors

E Schulze-Lohoff1, S Schagerl, A Ogilvie

  • 1Medizinische Klinik IV, Universität Erlangen-Nürnberg, Germany.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|November 1, 1995
PubMed
Abstract

Insights

Extracellular adenosine triphosphate (ATP) significantly enhances glomerular mesangial cell (MC) growth when combined with various growth factors. This synergistic effect suggests ATP may play a role in kidney diseases like glomerulonephritis.

Area of Science:

  • Cell Biology
  • Renal Physiology
  • Molecular Signaling

Background:

  • Extracellular adenosine triphosphate (ATP) is released during tissue injury and platelet aggregation.
  • ATP exhibits a modest mitogenic effect on cultured rat glomerular mesangial cells (MCs).

Purpose of the Study:

  • Investigate the interaction of ATP with multiple growth factors in MC mitogenesis.
  • Determine the synergistic effects of ATP on MC proliferation.

Main Methods:

  • Measured MC replication via direct cell counting.
  • Assessed DNA synthesis using 3H-thymidine uptake.
  • Quantified phosphatidylinositol-specific phospholipase C (PI-PLC) activity by measuring inositol phosphate formation.

Main Results:

  • Extracellular ATP (1-100 microM) powerfully synergized with EGF, bFGF, PDGF-BB, ET-1, AVP, Thr, 5-HT, and IL-1 beta to increase MC DNA synthesis.
  • ATP augmented MC growth induced by these factors without altering their half-maximal concentrations.
  • ATP activated PI-PLC, but this activation was not essential for ATP's synergistic mitogenic effect with growth factors.

Conclusions:

  • Extracellular ATP synergistically augments MC growth stimulated by multiple growth factors.
  • The precise ATP-induced mitogenic signaling pathway remains to be elucidated.
  • ATP may contribute to the pathogenesis of glomerulonephritis due to its interaction with growth factors released during inflammation.

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