title: Prostaglandin F2alpha potentiates the calcium dependent activation of mitochondrial metabolism in luteal cells.
abstract: 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, PGF2alpha 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 PGF2alpha than to ATP. PGF2alpha more effectively increased NAD(P)H level also in mouse luteal cells. PGF2alpha 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 PGF2alpha and ATP. Raising [Ca2+]c with ionomycin increased the NAD(P)H signal, which was further raised by PGF2alpha but not by ATP. These data suggest that PGF2alpha 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.
authors.affiliation: Laboratory of Cellular and Molecular Physiology, Department of Physiology, Semmelweis University and Hungarian Academy of Sciences, P.O. Box 259, H-1444 Budapest, Hungary.
authors.forename: János G
authors.initials: JG
authors.lastname: Pitter
authors.forename: Gergo
authors.initials: G
authors.lastname: Szanda
authors.forename: Michael R
authors.initials: MR
authors.lastname: Duchen
authors.forename: András
authors.initials: A
authors.lastname: Spät
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D002952:Citric Acid Cycle / Q000187:drug effects / Q000502:physiology; D003338:Corpus Luteum / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015237:Dinoprost / Q000378:metabolism* / Q000494:pharmacology; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005260:Female; D015759:Ionomycin / Q000494:pharmacology; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009249:NADP / Q000378:metabolism; D009250:NADP Transhydrogenases / Q000187:drug effects / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D018048:Receptors, Purinergic P2 / Q000187:drug effects / Q000378:metabolism; D012402:Rotenone / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D018048:Receptors, Purinergic P2; D012402:Rotenone; D009249:NADP; D015759:Ionomycin; D000255:Adenosine Triphosphate; D015237:Dinoprost; D009250:NADP Transhydrogenases; D002118:Calcium