Cross-regulation of novel protein kinase C (PKC) isoform function in cardiomyocytes. Role of PKC epsilon in activation loop phosphorylations and PKC delta in hydrophobic motif phosphorylations

J Biol Chem. 2003 Apr 18;278(16):14555-64. doi: 10.1074/jbc.M212644200. Epub 2003 Jan 31.

Abstract

Recent studies identify conventional protein kinase C (PKC) isoform phosphorylations at conserved residues in the activation loop and C terminus as maturational events that influence enzyme activity and targeting but are not dynamically regulated by second messengers. In contrast, this study identifies phorbol 12-myristoyl 13-acetate (PMA)- and norepinephrine-induced phosphorylations of PKC epsilon (at the C-terminal hydrophobic motif) and PKC delta (at the activation loop) as events that accompany endogenous novel PKC (nPKC) isoform activation in neonatal rat cardiomyocytes. Agonist-induced nPKC phosphorylations are prevented (and the kinetics of PMA-dependent PKC down-regulation are slowed) by pharmacologic inhibitors of nPKC kinase activity. PKC delta is recovered from PMA-treated cultures with increased in vitro lipid-independent kinase activity (and altered substrate specificity); the PMA-dependent increase in PKC delta kinase activity is attenuated when PKC delta activation loop phosphorylation is prevented. To distinguish roles of individual nPKC isoforms in nPKC phosphorylations, wild-type (WT) and dominant negative (DN) PKC delta and PKC epsilon mutants were introduced into cardiomyocyte cultures using adenovirus-mediated gene transfer. WT-PKC delta and WT-PKC epsilon are highly phosphorylated at activation loop and hydrophobic motif sites, even in the absence of allosteric activators. DN-PKC delta is phosphorylated at the activation loop but not the hydrophobic motif; DN-PKC epsilon is phosphorylated at the hydrophobic motif but not the activation loop. Collectively, these results identify a role for PKC epsilon in nPKC activation loop phosphorylations and PKC delta in nPKC hydrophobic motif phosphorylations. Agonist-induced nPKC isoform phosphorylations that accompany activation/translocation of the enzyme contribute to the regulation of PKC delta kinase activity, may influence nPKC isoform trafficking/down-regulation, and introduce functionally important cross-talk for nPKC signaling pathways in cardiomyocytes.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenoviridae / genetics
  • Allosteric Site
  • Amino Acid Motifs
  • Animals
  • Cells, Cultured
  • Conserved Sequence
  • Down-Regulation
  • Gene Expression Regulation, Enzymologic
  • Gene Transfer Techniques
  • Genes, Dominant
  • Immunoblotting
  • Kinetics
  • Models, Biological
  • Myocardium / cytology*
  • Phosphorylation
  • Protein Isoforms
  • Protein Kinase C / chemistry*
  • Protein Kinase C / metabolism
  • Protein Kinase C / physiology*
  • Protein Kinase C-delta
  • Protein Kinase C-epsilon
  • Protein Transport
  • Rats
  • Rats, Wistar
  • Signal Transduction
  • Substrate Specificity
  • Time Factors
  • Transfection

Substances

  • Protein Isoforms
  • Prkcd protein, rat
  • Prkce protein, rat
  • Protein Kinase C
  • Protein Kinase C-delta
  • Protein Kinase C-epsilon