Prostaglandin F potentiates the calcium dependent activation of mitochondrial metabolism in luteal cells

János G. Pitter, Gergo Szanda, Michael R. Duchen, András Spät

Research output: Contribution to journalArticle

9 Citations (Scopus)


Cytoplasmic Ca2+ signals are transferred to the mitochondria and activate the Krebs cycle. We have compared the efficiency of this process for two Ca2+ mobilising agonists, PGF and ATP (acting at metabotropic P2 receptors) in rat luteal cells. [Ca2+]c, [Ca2+]m and mitochondrial NAD(P)H were monitored by means of microspectrofluorimetry and confocal microscopy. While both agonists caused similar elevations of [Ca2+]c, changes in NAD(P)H were larger in response to PGF than to ATP. PGF more effectively increased NAD(P)H level also in mouse luteal cells. PGF caused a faster rate of rise of NAD(P)H fluorescence than ATP when reoxidation was prevented with rotenone, suggesting a faster rate of NAD(P)+ reduction. The NAD(P)H response to both agonists was dependent on the mobilisation of stored Ca2+. We found no difference in the efficacy of transmission of the [Ca2+]c signal to mitochondria in response to PGF and ATP. Raising [Ca2+]c with ionomycin increased the NAD(P)H signal, which was further raised by PGF but not by ATP. These data suggest that PGF potentiates the Ca2+-induced stimulation of mitochondrial metabolism by a Ca2+-independent mechanism and shows that agonists may modulate mitochondrial function differentially through a novel process beyond the simple transfer of Ca2+ from ER to mitochondria.

Original languageEnglish
Pages (from-to)35-44
Number of pages10
JournalCell Calcium
Issue number1
Publication statusPublished - Jan 2005


  • ATP
  • Calcium
  • Luteal cell
  • Mitochondria
  • NADH
  • Prostaglandin F
  • Pyridine nucleotide

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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