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Antiproliferative effect of UTP on human arterial and venous smooth muscle cells

P J White1, R Kumari, K E Porter

  • 1Cell Signalling Laboratory, Department of Biological Sciences, De Montfort University, Leicester LE1 9BH.

Insights

Extracellular nucleotides like UTP regulate vascular smooth muscle cell proliferation. UTP inhibits platelet-derived growth factor-stimulated proliferation in human vascular smooth muscle cells, acting as an anti-proliferative agent.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Physiology

Background:

  • Extracellular nucleotides, including adenosine triphosphate (ATP) and uridine triphosphate (UTP), play diverse roles in cellular signaling.
  • Vascular smooth muscle cells (VSMC) are crucial for regulating blood vessel tone and structure.
  • Understanding the regulation of VSMC proliferation is vital for cardiovascular health.

Purpose of the Study:

  • To investigate the role of extracellular nucleotides (ATP and UTP) in regulating proliferation of human vascular smooth muscle cells (VSMC).
  • To determine if ATP and UTP influence cell proliferation stimulated by platelet-derived growth factor (PDGF).

Main Methods:

  • Cultured human VSMC from internal mammary artery (IMA) and saphenous vein (SV) were used.
  • Measurements included cytosolic free Ca(2+) concentration ([Ca(2+)](i)) and [(3)H]thymidine incorporation into DNA.
  • Cell proliferation and mitogen-activated protein kinase (MAPK) cascade activation were assessed.

Main Results:

  • ATP and UTP increased [Ca(2+)](i) in both IMA- and SV-derived VSMC.
  • ATP enhanced PDGF-stimulated [(3)H]thymidine incorporation in SV-derived cells only.
  • UTP inhibited PDGF-stimulated [(3)H]thymidine incorporation and cell proliferation in both IMA- and SV-derived VSMC, independent of MAPK signaling.

Conclusions:

  • UTP acts as an anti-proliferative regulator in human VSMC of both arterial and venous origin.
  • Extracellular nucleotides differentially modulate VSMC proliferation responses.
  • UTP's anti-proliferative effect is not mediated through the p42/p44 MAPK cascade.

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