Paracrine communication between mechanically stretched myocytes and fibroblasts

Methods Mol Biol. 2013:1066:57-66. doi: 10.1007/978-1-62703-604-7_5.

Abstract

Mechanical stretch is a major factor for myocardial hypertrophy and heart failure. Stretch activates mechanical sensors from cardiac myocytes, leading to a series of signal transduction cascades, which can result in cell malfunction and remodeling. It is well known that mechanical stretch also induces the release of paracrine factors from cardiac fibroblasts, as well as myocytes. Due to complicated circumstance of heart tissue, it is difficult to fully investigate the characteristics of these factors in situ. Here we describe static stretch and conditioned medium experiments as methods to examine the function of paracrine factors between primary cultured cardiac myocytes and fibroblasts.

Publication types

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

MeSH terms

  • Animals
  • Cardiomegaly
  • Cells, Cultured
  • Centrifugation, Density Gradient
  • Extracellular Matrix / metabolism
  • Fibroblasts / physiology*
  • Heart / physiology
  • MAP Kinase Signaling System
  • Mitogen-Activated Protein Kinases / metabolism
  • Muscle Proteins / metabolism
  • Myocytes, Cardiac / physiology*
  • Paracrine Communication / physiology*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Stress, Mechanical*

Substances

  • Muscle Proteins
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases