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Phospholipase A(2) is involved in thapsigargin-induced sodium influx in human lymphocytes

J R Nofer1, R Junker, M Walter

  • 1Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Westfälische Wilhelms-Universität, A. Schweitzer Str 33, Münster, 48-149, Germany.

Archives of Biochemistry and Biophysics
|February 10, 2000
PubMed

Insights

Thapsigargin triggers sodium (Na+) influx in human lymphocytes by activating phospholipase A2 (PLA2), a process dependent on tyrosine kinase signaling. This finding reveals a novel mechanism for ion transport in immune cells.

Area of Science:

  • Cellular Physiology
  • Immunology
  • Biochemistry

Background:

  • Previous research indicated that thapsigargin, an inhibitor of the endoplasmic Ca(2+)-ATP-ase, causes Na+ influx in human lymphocytes.
  • The precise mechanism behind this thapsigargin-induced Na+ entry remained unclear.

Purpose of the Study:

  • To elucidate the underlying mechanism of thapsigargin-induced Na+ influx in human lymphocytes.
  • To investigate the role of phospholipase A2 (PLA2) and tyrosine kinase signaling in this process.

Main Methods:

  • Utilized phospholipase A2 (PLA2) inhibitors (p-bromophenacyl bromide, OBAA, BEL) to assess their effect on thapsigargin-induced Na+ influx.
  • Investigated the impact of exogenously added PLA2 and arachidonic acid (AA) on Na+ concentration.
  • Examined the role of tyrosine kinase inhibitor genistein and extracellular Ca2+ in the observed phenomena.

Main Results:

  • Thapsigargin-induced Na+ influx was significantly inhibited by PLA2 inhibitors.
  • Exogenous PLA2 mimicked the Na+ influx, and thapsigargin stimulated arachidonic acid (AA) formation.
  • Both thapsigargin-induced Na+ influx and AA liberation were dependent on tyrosine kinase activity but not extracellular Ca2+.

Conclusions:

  • Thapsigargin-induced Na+ entry in human lymphocytes is mediated by the activation of phospholipase A2 (PLA2).
  • This process is intrinsically linked to tyrosine kinase-dependent signaling pathways.
  • The findings highlight a novel mechanism involving PLA2 and tyrosine kinases in regulating ion flux in lymphocytes.

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