Activation of PKC induces leukocyte adhesion by the dephosphorylation of ERM

Kouichi Tachibana1, Hiroe Ohnishi2, Seyed Mohammad Ali Haghparast3

  • 1Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 1-1-1 Higashi, Tsukuba, Ibaraki, 305-8562, Japan.

Insights

External stimuli trigger leukocyte adhesion by dephosphorylating Ezrin/Radixin/Moesin (ERM) proteins, a process involving Protein Kinase C (PKC). This dephosphorylation is crucial for the switch from non-adherent to adherent states in leukocytes.

Area of Science:

  • Cell Biology
  • Immunology
  • Biochemistry

Background:

  • Circulating leukocytes are typically non-adherent but can adhere upon stimulation.
  • Understanding the molecular mechanisms of this adhesion switch is critical in immunology.

Purpose of the Study:

  • To investigate the mechanism of PMA-induced leukocyte adhesion.
  • To elucidate the role of Ezrin/Radixin/Moesin (ERM) proteins in leukocyte adhesion.

Main Methods:

  • Investigated PMA-induced cell adhesion in myelomonocytic KG-1 cells.
  • Analyzed changes in cell surface properties and protein phosphorylation.
  • Utilized PKC inhibitors and phosphatase inhibitors.

Main Results:

  • PMA induced leukocyte adhesion, characterized by microvillus collapse and decreased cell surface rigidity.
  • Adhesion events correlated with the dephosphorylation of Ezrin/Radixin/Moesin (ERM) proteins.
  • Inhibition of ERM dephosphorylation or PKC activity blocked PMA-induced adhesion.

Conclusions:

  • External stimuli, such as PMA, induce leukocyte adhesion via Protein Kinase C (PKC)-mediated dephosphorylation of ERM proteins.
  • ERM dephosphorylation is a key event that facilitates the transition of leukocytes from a non-adherent to an adherent state.

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