Regulation of endothelin-1 expression in the bovine corpus luteum: elevation by prostaglandin F 2 alpha.

Girsh, Eliezer; Wang, W; Mamluk, Roni; Arditi, F; Friedman, Ahuva; Milvae, R. A.; Meidan, Rina

doi:10.1210/endo.137.12.8940334

Cited by 87 publications

(56 citation statements)

References 43 publications

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“…Additionally, as demonstrated in this study, luteal endothelial cells are the predominant site of ppET-1 and NOS mRNA expression, therefore levels found in endothelial cells are indicative of tissue levels. Indeed, our findings in endothelial cells are corroborated by data available on iNOS and ET-1 in corpora lutea of mid cycle (Girsh et al 1996, Milvae 2000, Skarzynski et al 2003. Of particular interest are the inverse relationship between ppET-1 and iNOS observed here.…”

Section: Discussionsupporting

confidence: 90%

“…The compound(s) emanating from the corpus luteum milieu which is responsible for the elevated iNOS expression in freshly isolated endothelial cells is at present unknown. Yet, the fact that iNOS is already elevated in luteal tissue at the mid-late luteal phase (Skarzynski et al 2003) and in endothelial cells of mid cycle (this study) when ET-1 expression is still low (Girsh et al 1996, Milvae 2000 and this study) may suggest that NO regulates steady state luteal function. ET-1, in contrast, is not elevated until luteolysis commences (Girsh et al 1996, Hinckley & Milvae 2001) and therefore would be expected to act mainly during luteolysis.…”

Section: Discussionmentioning

confidence: 59%

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Characterization of endothelin-1 and nitric oxide generating systems in corpus luteum-derived endothelial cells

Klipper

Gilboa²,

Levy³

et al. 2004

Reproduction

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Endothelium-derived endothelin-1 (ET-1) and nitric oxide (NO) are pivotal regulators of corpus luteum (CL) function. To have a better insight into their synthesis and action, members of the ET system (ET-1, ET converting enzyme (ECE-1) isoforms a -d, ET A and ET B receptors) along with NO synthase (NOS) isoforms -endothelial (e)NOS and inducible (i)NOS -were quantified in CL-derived endothelial cells (CLEC). The expression of these genes in microvascular CLEC, obtained by lectin-coated magnetic beads, was compared with cells removed from the luteal microenvironment and maintained in culture for different durations, and with endothelial cells (EC) derived from a large blood vessel (i.e. bovine aortic endothelial cells, BAEC). The profile of gene expression in the different EC types was determined by quantitative real-time PCR. Freshly isolated EC from mid-cycle CL exhibited high ET-1 receptor expression (both ET A and ET B ), low ET-1 synthesizing ability (both prepro (pp) ET-1 and ECE-1), but elevated iNOS -the high throughput NOS isoform. The distinct phenotype of CLEC was lost soon after an overnight culture. ET A and ET B receptor levels declined, ppET-1 levels increased while iNOS was reduced. These changes were extenuated during long-term culture of CLEC. The general pattern of gene expression in BAEC and long-term cultured CLEC was similar yet some differences, reminiscent of freshly isolated CLEC, remained: ECE-1c, ET B receptor and NOS isoforms were expressed differently in BAEC as compared with lines of CLEC. This study suggests that the luteal microenvironment is necessary to sustain the selective phenotype of its resident endothelial cells. The inverse relationship between ppET-1 and iNOS observed in freshly isolated CLEC and in cultured cells is physiologically significant and suggests that ET-1 and NO may modulate the production of each other.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 59%

Characterization of endothelin-1 and nitric oxide generating systems in corpus luteum-derived endothelial cells

Klipper

Gilboa²,

Levy³

et al. 2004

Reproduction

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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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“…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: 98%

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.

show abstract

Regulation of endothelin-1 expression in the bovine corpus luteum: elevation by prostaglandin F 2 alpha.

Cited by 87 publications

References 43 publications

Characterization of endothelin-1 and nitric oxide generating systems in corpus luteum-derived endothelial cells

Characterization of endothelin-1 and nitric oxide generating systems in corpus luteum-derived endothelial cells

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..

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