TM-25659 enhances osteogenic differentiation and suppresses adipogenic differentiation by modulating the transcriptional co-activator TAZ

Br J Pharmacol. 2012 Mar;165(5):1584-94. doi: 10.1111/j.1476-5381.2011.01664.x.

Abstract

Background and purpose: The transcriptional co-activator with PDZ-binding motif (TAZ) is characterized as a transcriptional modulator of mesenchymal stem cell differentiation into osteoblasts and adipocytes. Moreover, increased TAZ activity in the nucleus enhances osteoblast differentiation and suppresses adipocyte development by interacting with runt-related transcription factor 2 (RUNX2) and PPARγ, respectively. Therefore, it would be of interest to identify low MW compounds that modulate nuclear TAZ activity.

Experimental approach: High-throughput screening was performed using a library of low MW compounds in order to identify TAZ modulators that enhance nuclear TAZ localization. The effects and molecular mechanisms of a TAZ modulator have been characterized in osteoblast and adipocyte differentiation.

Key results: We identified 2-butyl-5-methyl-6-(pyridine-3-yl)-3-[2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl]-3H-imidazo[4,5-b]pyridine] (TM-25659) as a TAZ modulator. TM-25659 enhanced nuclear TAZ localization in a dose-dependent manner and attenuated PPARγ-mediated adipocyte differentiation by facilitating PPARγ suppression activity of TAZ. In addition, TAZ-induced RUNX2 activity activation was further increased in osteoblasts, causing increased osteoblast differentiation. Accordingly, TM-25659 suppressed bone loss in vivo and decreased weight gain in an obesity model. After oral administration, TM-25659 had a favourable pharmacokinetic profile.

Conclusion and implications: TM-25659 stimulated nuclear TAZ localization and thus caused TAZ to suppress PPARγ-dependent adipogenesis and enhance RUNX2-induced osteoblast differentiation in vitro and in vivo. Our data suggest that TM-25659 could be beneficial in the control of obesity and bone loss.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipogenesis / drug effects*
  • Adipogenesis / genetics
  • Animals
  • Bone Resorption / drug therapy
  • Bone Resorption / genetics
  • Bone Resorption / metabolism
  • Bridged Bicyclo Compounds, Heterocyclic / pharmacology*
  • COS Cells
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Cell Nucleus
  • Cells, Cultured
  • Chlorocebus aethiops
  • Core Binding Factor Alpha 1 Subunit / metabolism
  • HEK293 Cells
  • Humans
  • Male
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Osteoblasts / cytology
  • Osteoblasts / drug effects
  • Osteoblasts / metabolism
  • Osteogenesis / drug effects*
  • Osteogenesis / genetics
  • PPAR gamma / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Small Molecule Libraries
  • Tetrazoles / pharmacology*
  • Trans-Activators
  • Weight Gain / drug effects
  • Weight Gain / genetics

Substances

  • 2-butyl-5-methyl-6-(pyridine-3-yl)-3-(2'-(1H-tetrazole-5-yl)-biphenyl-4-ylmethyl)-3H-imidazo(4,5-b)pyridine
  • Adaptor Proteins, Signal Transducing
  • Bridged Bicyclo Compounds, Heterocyclic
  • Core Binding Factor Alpha 1 Subunit
  • PPAR gamma
  • Small Molecule Libraries
  • Tetrazoles
  • Trans-Activators
  • Wwtr1 protein, mouse