AKAP-Lbc mobilizes a cardiac hypertrophy signaling pathway

Mol Cell. 2008 Oct 24;32(2):169-79. doi: 10.1016/j.molcel.2008.08.030.

Abstract

Elevated catecholamines in the heart evoke transcriptional activation of the Myocyte Enhancer Factor (MEF) pathway to induce a cellular response known as pathological myocardial hypertrophy. We have discovered that the A-Kinase Anchoring Protein (AKAP)-Lbc is upregulated in hypertrophic cardiomyocytes. It coordinates activation and movement of signaling proteins that initiate MEF2-mediated transcriptional reprogramming events. Live-cell imaging, fluorescent kinase activity reporters, and RNA interference techniques show that AKAP-Lbc couples activation of protein kinase D (PKD) with the phosphorylation-dependent nuclear export of the class II histone deacetylase HDAC5. These studies uncover a role for AKAP-Lbc in which increased expression of the anchoring protein selectively amplifies a signaling pathway that drives cardiac myocytes toward a pathophysiological outcome.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 14-3-3 Proteins / metabolism
  • A Kinase Anchor Proteins / genetics
  • A Kinase Anchor Proteins / metabolism
  • A Kinase Anchor Proteins / physiology*
  • Active Transport, Cell Nucleus
  • Animals
  • COS Cells
  • Cardiomegaly / metabolism*
  • Cell Line
  • Chlorocebus aethiops
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Gene Expression Regulation
  • Guanine Nucleotide Exchange Factors / genetics
  • Guanine Nucleotide Exchange Factors / metabolism
  • Guanine Nucleotide Exchange Factors / physiology*
  • Heart Ventricles / drug effects
  • Histone Deacetylases / metabolism
  • Humans
  • MEF2 Transcription Factors
  • Minor Histocompatibility Antigens
  • Models, Biological
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Myogenic Regulatory Factors / metabolism
  • Phenylephrine / pharmacology
  • Phosphorylation
  • Protein Kinase C / metabolism
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins / physiology*
  • RNA Interference
  • Rats
  • Signal Transduction*

Substances

  • 14-3-3 Proteins
  • A Kinase Anchor Proteins
  • AKAP13 protein, human
  • Guanine Nucleotide Exchange Factors
  • MEF2 Transcription Factors
  • Minor Histocompatibility Antigens
  • Myogenic Regulatory Factors
  • Proto-Oncogene Proteins
  • Phenylephrine
  • protein kinase D
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase C
  • Hdac5 protein, rat
  • Histone Deacetylases