PGE2 suppresses mitogen-induced Ca2+ mobilization in T cells

Mashkoor A. Choudhry, Philip E. Hockberger, Mohammed M. Sayeed*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


PGE2- mediated suppression of T cell proliferation during sepsis could result from altered Ca2+ signaling. The present study evaluated the effects of PGE2 on Ca2+ release from intracellular stores and its influx through the plasma membrane in splenic T cells from Sprague-Dawley rats. Intracellular Ca2+ concentration ([Ca2+](i)) responses in individual T cells were assessed using the Ca2+ imaging technique, and the release of Ca2+ from intracellular stores and Ca2+ influx were spectrofluorometrically quantified in T cell suspensions. Under unstimulated conditions, nearly 85% of T cells exhibited [Ca2+](i) ≤50 nM. After stimulation with concanavalin A (Con A), an increase in [Ca2+](i) was recorded in ~60% of the cells. The pretreatment oft cells with PGE2 had no apparent effect on [Ca2+](i) in resting cells; it significantly suppressed the Con A-induced increase in [Ca2+](i) in all of the Con A-responsive cells. Ca2+ release from the intracellular stores contributed to the early spike in [Ca2+](i), and the late phase of elevation in [Ca2+](i) was dependent on Ca2+ influx through the plasma membrane. Our data suggest that PGE2 causes an overall suppression of the Con A-induced [Ca2+](i) elevation in T cells via inhibiting both Ca2+ influx and its release from the intracellular stores.

Original languageEnglish (US)
Pages (from-to)R1741-R1748
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number6 46-6
StatePublished - Dec 1999


  • Adenosine 3,5-cyclic monophosphate
  • Calcium ion signaling
  • Concanavalin A
  • Intracellular calcium ion release
  • Prostaglandin E
  • T lymphocytes

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology


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