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Epidermal growth factor modulates release of arachidonic acid from embryonic cells

K P Chepenik1

  • 1Department of Anatomy, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.

Lipids
|September 1, 1989
PubMed

Insights

Calcium ionophore A23187 releases arachidonic acid from growing MEPM cells. Pretreatment with EGF or PMA enables release from confluent cells, suggesting protein kinase C modulates phospholipid hydrolase activity.

Area of Science:

  • Cell biology
  • Biochemistry
  • Molecular signaling

Background:

  • Arachidonic acid release is a key signaling event.
  • MEPM cells exhibit differential responses to calcium ionophores based on growth state.
  • Epidermal Growth Factor (EGF) and Phorbol 12-myristate 13-acetate (PMA) are known activators of protein kinase C.

Purpose of the Study:

  • To investigate the role of protein kinase C in regulating [3H]arachidonic acid release in MEPM cells.
  • To determine if EGF or PMA can overcome the inhibition of arachidonic acid release in confluent MEPM cells.

Main Methods:

  • Radiolabeling of MEPM cells with [3H]arachidonic acid.
  • Stimulation of cells with calcium ionophore A23187.
  • Pretreatment of confluent cells with EGF or PMA.
  • Measurement of released [3H]arachidonic acid.

Main Results:

  • A23187 stimulated [3H]arachidonic acid release from growing MEPM cells, but not confluent cells.
  • Pretreatment with EGF or PMA enabled A23187-induced [3H]arachidonic acid release from confluent MEPM cells.
  • EGF and PMA alone did not stimulate [3H]arachidonic acid release, but activated protein kinase C.

Conclusions:

  • Protein kinase C activation is necessary for EGF/PMA-induced modulation of phospholipid hydrolase activity in MEPM cells.
  • These findings support a model where protein kinase C plays a crucial role in regulating arachidonic acid release pathways in MEPM cells.

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