T0901317, an LXR agonist, augments PKA-induced vascular cell calcification

FEBS Lett. 2009 Apr 17;583(8):1344-8. doi: 10.1016/j.febslet.2009.03.039. Epub 2009 Mar 25.

Abstract

We examined the effect of liver X receptor (LXR) agonists on vascular calcification, prevalent in atherosclerotic lesions. T0901317, an LXR agonist, augmented protein kinase A (PKA)-induced mineralization and alkaline phosphatase (ALP) activity in aortic smooth muscle cells isolated from wild-type, but not from Lxrbeta(-/-)mice. A six-hour T0901317 treatment augmented the PKA-induced expression of the phosphate transporter Pit-1, a positive regulator of mineralization, suggesting a direct role. A ten-day T0901317 treatment attenuated PKA-induced expression of mineralization inhibitors, osteopontin and ectonucleotide pyrophosphatase/phosphodiesterase-1, suggesting an indirect role. The effects of T0901317 were attenuated by inhibition of ALP, Pit-1 and Rho-associated kinase, but not by inhibition of PKA. These results suggest that T0901317-augmented mineralization occurs downstream of PKA, involving both direct and indirect LXR-mediated pathways.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Calcinosis*
  • Cells, Cultured
  • Cyclic AMP-Dependent Protein Kinases / metabolism*
  • DNA Primers
  • DNA-Binding Proteins / agonists*
  • DNA-Binding Proteins / genetics
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / enzymology
  • Endothelium, Vascular / pathology
  • Hydrocarbons, Fluorinated / pharmacology*
  • Liver X Receptors
  • Mice
  • Mice, Knockout
  • Orphan Nuclear Receptors
  • Receptors, Cytoplasmic and Nuclear / agonists*
  • Receptors, Cytoplasmic and Nuclear / genetics
  • Sulfonamides / pharmacology*

Substances

  • DNA Primers
  • DNA-Binding Proteins
  • Hydrocarbons, Fluorinated
  • Liver X Receptors
  • Orphan Nuclear Receptors
  • Receptors, Cytoplasmic and Nuclear
  • Sulfonamides
  • T0901317
  • Cyclic AMP-Dependent Protein Kinases