Arachidonic acid inhibits hCG-stimulated progesterone production by corpora lutea of primates: Potential mechanism of action

Ciereszko, Renata E.; Guan, Zhen; Stokes, Bradford T.; Petroff, Brian K.; Ottobre, Ann C.; Ottobre, Joseph S.

doi:10.1016/0090-6980(95)00107-7

Cited by 9 publications

(6 citation statements)

References 51 publications

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“…The isoform of PKC has been shown to be present in porcine follicular and luteal tissue (DeManno et al 1992). In addition, some PKC isoforms may be activated by free fatty acids such as arachidonic acid generated by phospholipase A 2 (Ciereszko et al 1995, Liu 1996. The absence of any increase in [Ca 2+ ] i after treatment of luteal cells with PRL in the present study suggests that such calciumindependent mechanisms may be responsible for the observed PKC activation.…”

Section: Figurementioning

confidence: 39%

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Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs

Ciereszko

Petroff

Ottobre

et al. 1998

Journal of Endocrinology

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Previously, we reported that administration of prolactin (PRL) during the early luteal phase in sows increases plasma progesterone concentrations. In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the effect of PRL and/or low-density lipoproteins (LDL) on progesterone production by porcine luteal cells derived from early corpora lutea, and (2) to assess the ability of PRL to activate phosphoinositide-specific phospholipase C (PI-PLC) and protein kinase C (PKC) in these luteal cells. Ovaries with early corpora lutea (day 1-2 of the oestrous cycle) were obtained from the slaughterhouse. Progesterone production by dispersed luteal cells was measured after treatment with PRL, phorbol 12-myristate 13-acetate or inhibitors of PKC in the presence or absence of LDL. LDL increased progesterone concentration in the incubation medium (304·5 vs 178·6 ng/ml in control, P<0·05). PRL augmented LDL-stimulated progesterone secretion by luteal cells (to 416 ng/ml, P<0·05), but PRL alone did not affect progesterone production (209·6 ng/ml, P>0·05). Staurosporine, a PKC inhibitor, inhibited progesterone secretion stimulated by the combined action of LDL and PRL; however, such inhibition was not demonstrated when cells were treated with the PKC inhibitor, H-7. PKC activation was assessed by measuring the specific association of [ 3 H]phorbol dibutyrate ( 3 H-PDBu) with luteal cells after treatment with PRL or ionomycin (a positive control). PRL and ionomycin increased 3 H-PDBu-specific binding in early luteal cells by 28 5·5% (within 5 min) and 70·2 19·3% (within 2 min) over control binding respectively (P<0·05). In addition, PRL did not augment the LDLstimulated progesterone production in PKC-deficient cells. In contrast with PKC, total inositol phosphate accumulation, as well as intracellular free calcium concentrations, were not affected by PRL in the current study. We conclude that PRL, in the presence of LDL, stimulates progesterone production by early corpora lutea in vitro.Moreover, PRL appears to activate PKC, but not PI-PLC, in these cells. Thus intracellular transduction of the PRL signal may involve activation of PKC that is not dependent on PI-PLC.

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Section: Figurementioning

confidence: 39%

“…This technique has been used successfully to measure PKC activation in phagocytic cells (Dougherty & Niedel 1986, Walters et al 1992, and we have previously used it to measure PKC activation in primate luteal cells (Ciereszko et al 1995).…”

Section: Experimental Designmentioning

confidence: 99%

Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs

Ciereszko

Petroff

Ottobre

et al. 1998

Journal of Endocrinology

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“…However, there is evidence that PKC can modulate progestogen biosynthesis/neurosteroidogenesis in a number of model systems. In support, P production is stimulated in luteal cells of primates through the activation of PKC [6]. Additionally, PKC may target activity of the steroidogenic acute regulatory (StAR) protein which mediates transfer of cholesterol from the outer to the inner mitochondrial membrane, where it is converted by P450 side chain cleavage (P450 scc ) enzyme to pregnenolone (i.e.…”

Section: Discussionmentioning

confidence: 99%

Activity of protein kinase C is important for 3α,5α-THP's actions at dopamine type 1-like and/or GABAA receptors in the ventral tegmental area for lordosis of rats

Frye

Walf

2008

Brain Research Bulletin

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In the ventral tegmental area, progestogens facilitate sexual receptivity of rodents via actions at dopamine type 1-like and/or γ-aminobutyric type A receptors and activation of downstream signal transduction molecules. In the present study, we investigated whether effects of progesterone's metabolite, 3α,5α-THP, to enhance lordosis via actions at these receptors in the ventral tegmental area requires phospholipase C-dependent protein kinase C. The objective of this study was to test the hypothesis that: if progestogens' actions through dopamine type 1-like and/or γ-aminobutyric type A receptors in the ventral tegmental area for lordosis require protein kinase C, then inhibiting protein kinase C in the ventral tegmental area should reduce 3α,5α-THP-facilitated lordosis and its enhancement by dopamine type 1-like or γ-aminobutyric type A receptor agonists. Ovariectomized, E 2 (10 μg s.c. at hr 0)-primed rats were tested for their baseline lordosis responses and then received a series of three infusions to the ventral tegmental area: first, bisindolylmaleimide (75 nM/side) or vehicle; second, SKF38393 (100 ng/side), muscimol (100 ng/side), or vehicle; third, 3α,5α-THP (100, 200 ng) or vehicle. Rats were pre-tested for lordosis and motor behavior and then tested for lordosis after each infusion and 10 and 60 mins after the last infusion. Rats were tested for motor behavior following their last lordosis test. As has been previously demonstrated, 3α,5α-THP infusions to the ventral tegmental area increased lordosis and effects were further enhanced by infusions of SKF38393 and muscimol. Infusions of bisindolylmaleimide to the ventral tegmental area attenuated 3α,5α-THP-, SKF38393-, and/or muscimol-facilitated lordosis. Effects on lordosis were not solely due to changes in general motor behavior. Thus, 3α,5α-THP's actions in the ventral tegmental area through membrane receptors may require activity of protein kinase C.

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“…Moreover, the inhibition of PI hydrolysis suppressed steroid hormone secretion by porcine theca cells (Kaminski et al, 2003). The accumulation of IPs was also associated with an increase in P 4 production in luteal cells of primates and pigs (Ciereszko et al, 1995;Kaminski et al, 1999). It should be emphasised that, according to Yuan and Connor (1993), the activation of the PKC/[Ca 2+ ] i system can increase P 4 secretion by porcine luteal cells before the cells acquire luteolytic capacity.…”

Section: Discussionmentioning

confidence: 99%

“…After 36-38 h of culture, medium was collected, centrifuged (800 × g, 10 min) and stored at -20 °C until P 4 assay. Progesterone concentration was analysed by RIA (Ciereszko et al, 1995). The specificity of antibodies for P 4 has been reported previously (Ciereszko et al, 2001).…”

Section: The Effect Of Ot On Progesterone Releasementioning

confidence: 99%

The effect of oxytocin on progesterone secretion, phosphoinositide hydrolysis and intracellular mobilisation of Ca 2+ in porcine luteal cells

Franczak

Kurowicka

Kowalik

et al. 2009

Acta Veterinaria Hungarica

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Oxytocin (OT) is involved in the regulation of steroid secretion by the corpus luteum (CL) in pigs, but OT signal transduction in the porcine CL has not been identified. In this study, the effects of OT on in vitro progesterone (P 4 ) secretion, phosphoinositide (PI) hydrolysis and intracellular mobilisation of Ca 2+ ([Ca 2+ ] i ) were investigated in porcine luteal cells during the early (days 3-5), mid-(days 8-10) and late luteal phases (days 12-14) of the oestrous cycle. Basal concentrations of P 4 and accumulation of inositol phosphates (IPs) were higher (P < 0.05) on days 3-5 and 8-10 of the oestrous cycle than on days 12-14. Basal [Ca 2+ ] i mobilisation did not differ among studied periods of the oestrous cycle. Oxytocin (10 -7 M) enhanced P 4 secretion and PI hydrolysis (P < 0.05) by luteal cells harvested on days 8-10 of the oestrous cycle. Moreover, OT started to increase mobilisation of [Ca 2+ ] i at the 15th (days 3-5 and 8-10) or 30th second (days 12-14) in porcine luteal cells. It was concluded that in pigs OT acts as a regulator of steroidogenesis, stimulating P 4 secretion in mature CL. This OT action may be mediated by changes in PI hydrolysis and [Ca 2+ ] i mobilisation.

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Arachidonic acid inhibits hCG-stimulated progesterone production by corpora lutea of primates: Potential mechanism of action

Cited by 9 publications

References 51 publications

Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs

Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs

Activity of protein kinase C is important for 3α,5α-THP's actions at dopamine type 1-like and/or GABAA receptors in the ventral tegmental area for lordosis of rats

The effect of oxytocin on progesterone secretion, phosphoinositide hydrolysis and intracellular mobilisation of Ca 2+ in porcine luteal cells

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