Protein Kinase C Second Messenger System Mediates the Antisteroidogenic Effects of Prostaglandin F2α in the Ovine Corpus Luteum in Vivo1

McGuire, W J; Juengel, Jennifer L.; Niswender, Gordon D.

doi:10.1095/biolreprod51.4.800

Cited by 57 publications

(27 citation statements)

References 22 publications

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“…Stimulation of PKC in ovine large luteal cells was shown to be a dominant intracellular mechanism involved in progesterone suppression (Wiltbank et al 1990). This was confirmed later using the in vivo model in which an infusion of TPA into the ovarian artery also decreased plasma progesterone concentrations (McGuire et al 1994). Our present in vivo data further support this concept.…”

supporting

confidence: 86%

Local interaction of prostaglandin F2α with endothelin-1 and tumor necrosis factor-α on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade

Ohtani¹,

Takase²,

Wijayagunawardane³

et al. 2004

Reproduction

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Endothelin-1 (ET-1) and tumor necrosis factor-a (TNFa) participate in the cascade of luteolysis. Thus, in the present study the interactions of ET-1 and TNFa with prostaglandin F 2a (PGF 2a ) on the release of progesterone and oxytocin (OT) within the corpus luteum (CL) were investigated. A microdialysis system (MDS) was surgically implanted in ovine CL (one MDS line/CL; 5-10 lines/ewe) formed after super-ovulation. (1 mmol l 21 ), two consecutive perfusions of ET-1 decreased progesterone release more rapidly. Similarly, a pre-perfusion with PGF 2a followed by consecutive perfusions of ET-1 and then TNFa rapidly decreased progesterone release, with the inhibition most pronounced (35%) at 36 -48 h. The simultaneous infusion of ET-1 with PGF 2a induced a rapid decrease in progesterone release (36% at 36-48 h). In a further study, the possible second messenger systems involved in PGF 2a action on the release of progesterone, OT and ET-1 were investigated. A perfusion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA; 10 mmol l 21 ), A23187 (10 mmol l 21), or PGF 2a 1 A23187 increased progesterone release during infusion, but decreased it after perfusion. All treatments induced a massive release of OT during infusion, and increased ET-1 release after infusion. These results show that ET-1 is capable of suppressing progesterone release in the PGF 2a -primed ovine CL in vivo and thus ET-1 works as a local luteolysin together with PGF 2a during the process of functional luteolysis. During structural luteolysis, TNFa may interact with PGF 2a and ET-1 to cause a rapid drop in progesterone release and accelerate the process of luteolysis. This result supports the contention that ET-1 and TNFa interact with PGF 2a as local luteolytic mediators in the ewe as previously suggested.

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supporting

confidence: 86%

Local interaction of prostaglandin F2α with endothelin-1 and tumor necrosis factor-α on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade

Ohtani¹,

Takase²,

Wijayagunawardane³

et al. 2004

Reproduction

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“…PGF 2␣ -induced luteolysis is believed to be initiated through ligand receptor activation of the phospholipase C/diacylglycerol and inositol 1,4,5-trisphosphate (InsP 3 )/Ca 2ϩ -protein kinase C (PKC) signaling system (8 -10). This concept is supported by a number of reports demonstrating that the PKC activator phorbol myristate acetate (PMA) can in part mimic PGF 2␣ -induced luteolysis in vivo (11) and the actions of PGF 2␣ in vitro (12). However, a gap exists in our knowledge between the initial signaling events and the physiological sequelae observed in response to PGF 2␣ .…”

mentioning

confidence: 94%

Prostaglandin F2 Stimulates the Raf/MEK1/Mitogen-Activated Protein Kinase Signaling Cascade in Bovine Luteal Cells

Chen¹

1998

Endocrinology

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Upon binding to its G protein-coupled transmembrane receptors, the actions of PGF 2␣ on the corpus luteum are initiated by the phospholipase C/diacylglycerol-inositol 1,4,5-trisphosphate (InsP 3 )/Ca 2ϩ -protein kinase C (PKC) pathway. However, little is known about the downstream intracellular signaling events that can lead to transcriptional activation in response to PGF 2␣ . The present study was conducted to examine the involvement of the mitogen-activated protein kinase (MAPK) signaling cascade in the corpus luteum. Three isoforms of the Raf family of oncoprotein kinases (A-Raf, B-Raf, and Raf-1 or c-Raf) were detected in bovine luteal cells. Raf-1 and B-Raf, but not A-Raf, were activated by PGF 2␣ (1 M) and the pharmacological PKC activator phorbol myristate acetate (PMA, 20 nM). Kinetic analysis revealed that PGF 2␣ rapidly and transiently activated Raf-1.In vitro protein kinase assays demonstrated that activation of Raf-1 and B-Raf resulted in the phosphorylation and activation of MAPK kinase (MEK1), which subsequently phosphorylated p42 mapk . As determined by hyperphosphorylation, tyrosine phosphorylation, and enzymatic activity, p42 mapk and p44 mapk were rapidly and transiently activated by both PGF 2␣ (1 M) and PMA (20 nM 3876 -3885, 1998)

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“…In the present study, to investigate possible roles of NO in the process of apoptosis in the bovine CL, we studied (1) whether NO influences apoptosis signal transfer to cells by stimulating the expression of membrane receptor systems such as Fas LigandFas; (2) whether NO is engaged in gene expression of regulatory proteins, including proapoptotic Bax, provital Bcl-2 and caspase-3; and (3) whether NO influences [Ca 2+ ]i in bovine luteal cells.…”

mentioning

confidence: 99%

Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

Korzekwa

Okuda

Wocławek-Potocka

et al. 2006

Journal of Reproduction and Development

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Abstract. We previously showed in in vivo and in vitro studies that nitric oxide (NO) is engaged in luteolysis in cattle. Nitric oxide produced locally in the bovine corpus luteum (CL) inhibits progesterone (P4) synthesis and is suggested to be a component of the luteolytic cascade induced by uterine prostaglandin (PG) F2α. In the present study, the molecular mechanisms of NO action during structural luteolysis were studied in cultured bovine luteal cells (Days 15-17 of the estrous cycle). The effects of the NO donor (NONOate; 10 -4 M) on DNA fragmentation, cell viability, P4 production and caspase-3 activity were compared with those of PGF2α (10 -6 M). Moreover, mobilization of intracellular calcium [Ca 2+ ]i and gene expressions of Fas-L, Fas, bcl-2, bax, and caspase-3 in the cells were determined by semi-quantitative RT-PCR after NONOate treatment. Caspase-3 activity was examined calorimetrically. Contrary to PGF2α NONOate decreased cell viability. DNA fragmentation after NONOate treatment increased by more than with PGF22α. NONOate increased mobilization of [Ca 2+ ]i in the cells. Although the NO donor did not affect Fas-L and bcl-2 gene expression, it stimulated Fas and bax mRNA and caspase-3 expression. The ratio of bcl-2 to bax mRNA level decreased in the cells treated with NONOate. Moreover, NONOate stimulated caspase-3 activity more effectively than PGF2α. The overall results suggest that NO is a luteolytic factor that plays a crucial role in regulation of the estrous cycle in structural luteolysis by inducing apoptosis of luteal cells in cattle.

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Protein Kinase C Second Messenger System Mediates the Antisteroidogenic Effects of Prostaglandin F2α in the Ovine Corpus Luteum in Vivo1

Cited by 57 publications

References 22 publications

Local interaction of prostaglandin F2α with endothelin-1 and tumor necrosis factor-α on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade

Local interaction of prostaglandin F2α with endothelin-1 and tumor necrosis factor-α on the release of progesterone and oxytocin in ovine corpora lutea in vivo: a possible implication for a luteolytic cascade

Prostaglandin F2 Stimulates the Raf/MEK1/Mitogen-Activated Protein Kinase Signaling Cascade in Bovine Luteal Cells

Nitric Oxide Induces Apoptosis in Bovine Luteal Cells

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