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Fibroblast growth factor-2 stimulates phospholipase Cbeta in adult cardiomyocytes

P S Tappia1, R R Padua, V Panagia

  • 1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and Department of Human Anatomy & Cell Science, University of Manitoba, Winnipeg, Canada.

Insights

Fibroblast growth factor-2 (FGF-2) activates phosphoinositide-specific phospholipase C (PI-PLC) signaling pathways in adult cardiomyocytes. This research highlights FGF-2

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Cell Signaling

Background:

  • Fibroblast growth factor-2 (FGF-2) is recognized for its roles in cardiac protection and growth.
  • The specific signaling cascades initiated by FGF-2 in the adult heart remain incompletely understood.
  • Phosphoinositide-specific phospholipase C (PI-PLC) isozymes generate second messengers crucial for myocardial contractility and growth.

Purpose of the Study:

  • To investigate the effects of FGF-2 on PI-PLC isozyme activity in the adult heart.
  • To elucidate the signaling mechanisms underlying FGF-2's influence on cardiac cells.

Main Methods:

  • Isolated adult hearts were perfused with FGF-2.
  • Cytosolic inositol-1,4,5-trisphosphate levels and total PI-PLC activity were measured.
  • Membrane-associated PI-PLC isozyme activities (PLCγ1, PLCβ1) were assessed via immunoprecipitation.
  • Membrane levels of PLCβ1 and PLCβ3 were quantified.

Main Results:

  • FGF-2 administration increased cytosolic inositol-1,4,5-trisphosphate levels.
  • Total PI-PLC activity in sarcolemmal and cytosolic fractions was elevated by FGF-2.
  • FGF-2 induced a time-dependent increase in cardiomyocyte membrane-associated PLCγ1 and PLCβ1 activities.
  • Membrane levels of PLCβ1 and PLCβ3 were augmented following FGF-2 treatment.

Conclusions:

  • FGF-2 activates PI-PLC signaling pathways in adult cardiomyocytes.
  • The activation of PLCβ suggests crosstalk between FGF-receptor tyrosine kinase and G-protein-coupled signaling.
  • These findings underscore the significant role of FGF-2 in adult cardiac physiology.

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