Related Experiment Videos

Monensin-dependent and -independent mechanisms of cell-matrix adhesion

FEBS Letters
|December 2, 1985
PubMed

Insights

Cell spreading on subcellular matrix (SCM) is unaffected by monensin unless cells are iodinated. Iodination inactivates surface components, requiring a monensin-sensitive pathway for replacement from intracellular reserves.

Area of Science:

  • Cell Biology
  • Biochemistry

Background:

  • Cell adhesion and spreading are crucial processes mediated by cell surface components.
  • Understanding the regulation of these surface components is vital for cell biology research.

Purpose of the Study:

  • To investigate the role of intracellular reserves in cell spreading on subcellular matrix (SCM).
  • To determine the effect of surface iodination on cell spreading and its sensitivity to monensin.

Main Methods:

  • Human FL cells were cultured and treated to prepare SCM.
  • Cells were subjected to surface iodination using the lactoperoxidase/hydrogen peroxide (LPO/H2O2) system.
  • Cell adhesion and spreading assays were performed on SCM in the presence or absence of monensin.
  • Double-iodination experiments were conducted to assess receptor replenishment.

Main Results:

  • Cell attachment and spreading on SCM were insensitive to monensin in untreated cells.
  • Surface iodination of cells prior to adhesion inhibited spreading on SCM in a monensin-sensitive manner.
  • Double-iodination experiments showed an approximately 80% inhibition of cell spreading, suggesting inactivation of both existing and newly recruited surface receptors.

Conclusions:

  • Cell spreading on SCM relies on surface components that can be inactivated by iodination.
  • A monensin-sensitive pathway facilitates the replacement of inactivated surface components from intracellular reserves.
  • This pathway is essential when surface components are depleted or inactivated, as demonstrated by iodination experiments.

Related Concept Videos