The inhibitory mechanism of YC-1, a benzyl indazole, on smooth muscle cell proliferation: an in vitro and in vivo study

J Pharmacol Sci. 2004 Mar;94(3):252-60. doi: 10.1254/jphs.94.252.

Abstract

The pharmacological mechanisms of a synthetic compound 1-benzyl-3-(5'-hydroxymethyl-2'-furyl) indazole (YC-1) in preventing smooth muscle cell proliferation remains to be elucidated. The present study was aimed to explore the effects of YC-1 on certain molecules responsible for cell proliferation, including transforming growth factor (TGF)-beta1, soluble guanylyl cyclase (sGC) and focal adhesion kinase (FAK). The in vivo assay was correlated to the in vitro results of YC-1 on vascular stenosis. YC-1 was applied topically via a pluronic gel onto the balloon-injured rat carotid arteries, which were then harvested two weeks later for histological analysis. Our in vitro results showed that TGF-beta1 was suppressed by YC-1 by 50%. The translational level of sGC was threefold activated by YC-1 while the transcription level of sGC was increased up to 24-fold. FAK, the molecule responsible for cell proliferation and migration, was suppressed by YC-1 on the translational levels for 72%. These in vitro results were in consistent with the in vivo observation that the area ratio of neointima to media was reduced by YC-1. This study provides insights into the pharmacological mechanisms of YC-1 in preventing abnormal smooth muscle cell proliferation and thus supports the use of YC-1 as an adjuvant therapy for balloon injury-induced restenosis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Topical
  • Animals
  • Aorta, Thoracic / cytology
  • Aorta, Thoracic / drug effects
  • Carotid Artery, Common / pathology
  • Catheterization / adverse effects
  • Cell Division / drug effects*
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Glyceraldehyde-3-Phosphate Dehydrogenases / drug effects
  • Glyceraldehyde-3-Phosphate Dehydrogenases / genetics
  • Guanylate Cyclase / drug effects
  • Guanylate Cyclase / genetics
  • Guanylate Cyclase / metabolism
  • Imidazoles / chemistry
  • Imidazoles / pharmacology*
  • Indazoles / administration & dosage
  • Indazoles / chemistry
  • Indazoles / pharmacokinetics*
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / drug effects*
  • Muscle, Smooth, Vascular / growth & development
  • Poloxamer / chemistry
  • Poloxamer / metabolism
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Protein-Tyrosine Kinases / drug effects
  • Protein-Tyrosine Kinases / genetics
  • RNA, Messenger
  • Rats
  • Receptors, Enterotoxin
  • Receptors, Guanylate Cyclase-Coupled
  • Receptors, Peptide / drug effects
  • Receptors, Peptide / genetics
  • Receptors, Peptide / metabolism
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / metabolism
  • Tunica Intima / drug effects
  • Tunica Intima / growth & development
  • Tunica Intima / pathology

Substances

  • Imidazoles
  • Indazoles
  • RNA, Messenger
  • Receptors, Peptide
  • Transforming Growth Factor beta
  • Poloxamer
  • 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole
  • Glyceraldehyde-3-Phosphate Dehydrogenases
  • Protein-Tyrosine Kinases
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Ptk2 protein, rat
  • Guanylate Cyclase
  • Receptors, Enterotoxin
  • Receptors, Guanylate Cyclase-Coupled