Molecular mechanisms underlying PGF2alpha-induced hypertrophy of vascular smooth muscle cells

Yakugaku Zasshi. 2010 Feb;130(2):211-4. doi: 10.1248/yakushi.130.211.

Abstract

The present review focuses primarily on the studies we made in recent years to improve the understanding of the molecular mechanisms of PGF2alpha-induced hypertrophy of Vascular Smooth Muscle Cells (VSMC). In this review, we will summarize the recent findings in the context of the PGF2alpha signaling pathway in three parts: PGF2alpha binding to its receptor, transactivation of EGF receptor, two independent signaling transduction pathways increasing the expression of NOX1 gene.

Publication types

  • Review

MeSH terms

  • Activating Transcription Factor 1 / physiology
  • Animals
  • Dinoprost / metabolism
  • Dinoprost / physiology*
  • ErbB Receptors / genetics
  • Gene Expression Regulation
  • Humans
  • Hypertrophy
  • MADS Domain Proteins / physiology
  • MEF2 Transcription Factors
  • Muscle, Smooth, Vascular / cytology*
  • Muscle, Smooth, Vascular / pathology*
  • Myogenic Regulatory Factors / physiology
  • NADPH Oxidase 1
  • NADPH Oxidases / genetics
  • Phosphatidylinositol 3-Kinases / physiology
  • Protein Kinase C-delta / physiology
  • Receptors, Prostaglandin / metabolism
  • Signal Transduction / physiology*
  • Superoxides / metabolism
  • Transcriptional Activation
  • Up-Regulation
  • src-Family Kinases / physiology

Substances

  • Activating Transcription Factor 1
  • MADS Domain Proteins
  • MEF2 Transcription Factors
  • MEF2B protein, human
  • Myogenic Regulatory Factors
  • Receptors, Prostaglandin
  • prostaglandin F2alpha receptor
  • Superoxides
  • Dinoprost
  • NADPH Oxidase 1
  • NADPH Oxidases
  • NOX1 protein, human
  • Phosphatidylinositol 3-Kinases
  • ErbB Receptors
  • src-Family Kinases
  • Protein Kinase C-delta