Effect of endothelin-1 on bovine luteal cell function: role in prostaglandin F2alpha-induced antisteroidogenic action.

Girsh, Eliezer; Milvae, R. A.; Wang, W; Meidan, Rina

doi:10.1210/endo.137.4.8625904

Cited by 104 publications

(73 citation statements)

References 28 publications

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“…Namely, pre-exposure of the microenvironment within the bovine mid-CL with PGF2α potentiated the P inhibiting activity of endothelin-1 (ET-1) in the in vitro MDS model, which involves the activation of intracellular Ca 2+ . Consequently, we and others have proposed that a vasoactive peptide such as ET-1 mediates luteolytic actions of PGF2α in the bovine CL [17][18][19]. Recently, we have found that angio- tensin II is a possible additive luteolytic mediator in the bovine CL [20].…”

Section: Discussionmentioning

confidence: 91%

Direct Effect of PGF2.ALPHA., TPA and lonophore A23187 on Progesterone Release from Microdialyzed Corpus Luteum inthe Cow.

Ohtani

Kobayashi

Miyamoto

1999

Journal of Reproduction and Development

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Abstract. There is general agreement that prostaglandin F2α (PGF2α) is a physiological luteolysin in the cow. Contrary to this fact, PGF2α has been shown to stimulate the progesterone (P) release from luteal cells in vitro, through the activation of intracellular protein kinase C (PKC) and free calcium ion (Ca 2+ ). To examine the possibility that an essential factor or function(s) may be lost through the process of preparing cells from the corpus luteum (CL), we evaluated the direct effect of PGF2α, TPA and ionophore A23187 on local P release within the CL in the cow, by utilizing in vivo microdialysis system (MDS). Normal cyclic Holstein cows (n=4) were superovulated with FSH and the PGF2α analogue, and on Day 8 after estrus, they were surgically implanted with the MDS (cutoff Mr=1000 kDa) into multiple CL (1-3 line/CL). The system was continuously perfused with Ringer's solution from immediately after the surgery. On Days 10-11, several CL were assigned to the control, PGF2α (10 -5 M), TPA (10 -5 M), A23187 (10 -5 M), PGF2α+A23187 and TPA+A23187. The stimulants were infused into the CL using the MDS for 6 h, and each line of the MDS was further perfused with Ringer's solution for 26 h. A 6-h infusion with PGF2α stimulated P release during infusion, but after infusion the P release was again stable around the baseline. A 6-h infusion with TPA or A23187 strongly stimulated the P release. Similarly, PGF2α+A23187 or TPA+A23187 stimulated the P release. During the last 8 h of the experiment, A23187 alone, PGF2α+A23187 or TPA+A23187 inhibited the P release, whereas TPA as well as PGF2α maintained the same level as in the control. The results indicate that the direct exposure of the microenvironment in the bovine CL to PGF2α in vivo does not result in the suppression of P release until 26 h after stimulation, and that the activation of cytosolic free calcium is more effective in inhibiting the P release than the stimulation of PKC during the following period. Thus, the results support the concept that PGF2α needs some local luteolytic intermediator(s) that may enhance the intracellular calcium concentration.

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Section: Discussionmentioning

confidence: 91%

Direct Effect of PGF2.ALPHA., TPA and lonophore A23187 on Progesterone Release from Microdialyzed Corpus Luteum inthe Cow.

Ohtani

Kobayashi

Miyamoto

1999

Journal of Reproduction and Development

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“…These findings strongly suggest that the invasion of immune cells into the regressing CL is the major reason for the increase of TNF-α concentration in the CL at this period. Recently, we and others have shown that the production and release of endothelin-1, a vasoconstrictive peptide originated from endothelial cells, increased in the CL and ovarian venous plasma ipsilateral to the CL from 2 h after PGF2α injection in the cow, and proposed that endothelin-1 interacts with PGF2α as a local luteolytic factor [21][22][23][24]. It is likely that such vasoconstrictive peptides are responsible for an acute response to luteolytic PGF2α in both 1) direct inhibition of P release and 2) a vasoconstriction of arterioles, and thereby they can start an acute depletion of P release followed by a degeneration of CL tissue in which TNF-α plays a major role.…”

Section: Discussionmentioning

confidence: 96%

Intraluteal Release of Progesterone and Prostaglandins during PGF2.ALPHA.-Induced Luteolysis in Ewes: Local Effects of Tumor Necrosis Factor-.ALPHA..

Miyamoto

Nakatsuka

Ohtani

et al. 1998

Journal of Reproduction and Development

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Abstract. The role of tumor necrosis factor-α (TNF-α) in the local regulatory mechanisms of functional luteolysis in the ewe was examined. TNF-α was infused into a microdialysis system (MDS) implanted in the corpus luteum (CL) for 24 h from 2 h after the intramuscular injection of cloprostenol (defined as 0 h), and plasma as well as intraluteal changes of progesterone (P) and prostaglandins (PG) were observed. Three ewes were treated for superovulation, and multiple CL formed thereafter were surgically implanted with the MDS (1 line/CL) on Day 7 after GnRH injection. Serial fractions from the MDS were collected every 30 min for 40 h on Days 9-11 following a preperfusion period of 30 h. An intramuscular injection of cloprostenol stimulated an acute increase of plasma P concentration (an increase to 150%) within 1 h, followed by a rapid decrease within 6 h (P<0.05), which directly correlates with functional luteolysis. Intraluteal P release into the MDS showed a profile similar to that in the plasma, but significantly decreased from 17 h (P<0.05). Twenty-four-hour infusions of TNF-α at 20 ng/ml and 200 ng/ml into the MDS starting at 2 h after cloprostenol injection slightly hastened the time of onset of P decrease when they were compared with the time of the control. In contrast, the higher dose of TNF-α at 2000 ng/ml clearly delayed the time of onset of P decrease. Intraluteal release of PGF2α and PGE2 in the control was slightly increased between 18-32 h (P<0.05). A 26-h infusion with indomethacin partly blocked the increase in basal release of both PG (P<0.05), whereas it had no effect on the P release. A 24-h infusion with different concentrations of TNF-α stimulated the release of PGE2, but not the release of PGF2α (P<0.05). The results support the idea that TNF-α may have a passive or secondary role in functional luteolysis. Furthermore, the intraluteal PG production appears to have no direct correlation with functional luteolysis.

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“…Moreover, the administration of a luteolytic dose of PGF 2a rapidly stimulated gene expression for ET-1 in ovine CL collected at mid-cycle (Hinckley & Milvae 2001). It is likely, therefore, that ET-1 released from microvascular endothelial cells in the CL and luteal cells (Levy et al 2001, Schams et al 2003 cooperates with PGF 2a to initiate luteolysis by both directly inhibiting progesterone release (Girsh et al 1996a, Miyamoto et al 1997) via ETA-R (Girsh et al 1996a, Hinckley & Milvae 2001 and probably by vasoconstriction of arterioles that results in an acute drop in progesterone release.…”

Section: Introductionmentioning

confidence: 99%

“…Recent evidence in the cow suggests that endothelin-1 (ET-1), a vaso-constrictive 21-amino acid peptide, interacts with PGF 2a in the control of functional luteolysis (Girsh et al 1996a,b, Miyamoto et al 1997, Ohtani et al 1998, Meidan et al 1999. This hypothesis has been further supported by in vivo studies in the ewe.…”

Section: Introductionmentioning

confidence: 99%

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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Effect of endothelin-1 on bovine luteal cell function: role in prostaglandin F2alpha-induced antisteroidogenic action.

Cited by 104 publications

References 28 publications

Direct Effect of PGF2.ALPHA., TPA and lonophore A23187 on Progesterone Release from Microdialyzed Corpus Luteum inthe Cow.

Direct Effect of PGF2.ALPHA., TPA and lonophore A23187 on Progesterone Release from Microdialyzed Corpus Luteum inthe Cow.

Intraluteal Release of Progesterone and Prostaglandins during PGF2.ALPHA.-Induced Luteolysis in Ewes: Local Effects of Tumor Necrosis Factor-.ALPHA..

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

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