Control of progesterone production in small and large bovine luteal cells separated by flow cytometry

Alila, Hector W.; Dowd, Joseph P.; Corradino, R. A.; Harris, Whitney; Hansel, William

doi:10.1530/jrf.0.0820645

Cited by 121 publications

(75 citation statements)

References 26 publications

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“…These results would also support those of Rajkumar et al (1985Rajkumar et al ( , 1988 (Jordan, 1981;Pate & Condon, 1984;Kenny & Robinson, 1986;Benhaim et al, 1987;Alila et al, 1988;Pate & Nephew, 1988). Luteal cholesterol ester synthetase activity is inhibited and cholesterol ester stores are depleted by PGF2u ( Behrman et al, 1971).…”

Section: Cellular Uptake Of Lipoprotein-carried Cholesterolsupporting

confidence: 87%

Localization of prostaglandin F2 inhibition of lipoprotein use by bovine luteal cells

Grusenmeyer¹,

Pate²

1992

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Summary. Prostaglandin F2\g=a\(PGF2\g=a\) inhibits lipoprotein-stimulated progesterone production by bovine luteal cells in vitro and the objective of this study was to localize the site of action of PGF2\g=a\. Cultured bovine luteal cells were treated with PGF2\g=a\ for seven days, and then with either lipoproteins or 25-hydroxycholesterol in the presence of aminoglutethimide (which inhibits cholesterol side-chain cleavage) for the final 48 h. The effects of PGF2\g=a\ on progesterone production, cellular cholesterol content, mitochondrial cholesterol content and cholesterol side-chain cleavage activity were determined. As expected, PGF2\g=a\ inhibited (P < 0\m=.\05)lipoprotein-stimulated progesterone production. However, PGF2\g=a\ did not inhibit low-density lipoprotein-stimulated, or high density lipoprotein-stimulated, increases in cellular cholesterol (P < 0\m=.\05) or inhibit lipoprotein-induced increases in mitochondrial cholesterol content (P < 0\m=.\05). Additionally, cholesterol content of mitochondria increased (P < 0\m=.\05) in the presence of PGF2\g=a\ alone. To determine if the PGF2\g=a\-induced inhibition of steroidogenesis occurred at, or after, the side-chain cleavage reaction, we treated cells with the readily diffusable sterol, 25-hydroxycholesterol. Prostaglandin F2\g=a\ did not inhibit 25\ x=r eq-\ hydroxycholesterol-stimulated progesterone production (P < 0\m=.\05).Prostaglandin F2\ g=a\ may therefore exert its luteolytic effect at a site after cholesterol transport to the mitochondria but before cholesterol side-chain cleavage.

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Section: Cellular Uptake Of Lipoprotein-carried Cholesterolsupporting

confidence: 87%

Localization of prostaglandin F2 inhibition of lipoprotein use by bovine luteal cells

Grusenmeyer¹,

Pate²

1992

Reproduction

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“…8). PGF2 has been repeatedly shown to stimulate progesterone secretion of bovine CL in vitro (Hixon & Hansel 1979, Benhaim et al 1987, Alila et al 1988, Meidan et al 1992, Miyamoto et al 1993. A 30 min infusion of Ang II at 10 µmol/l following PGF2 continued to stimulate progesterone release.…”

Section: Discussionmentioning

confidence: 89%

Production and localisation of angiotensin II in the bovine early corpus luteum: a possible interaction with luteal angiogenic factors and prostaglandin F2 alpha

Kobayashi

Berisha²,

Amselgruber³

et al. 2001

Journal of Endocrinology

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The newly formed corpus luteum (CL) rapidly develops after ovulation and has the features of active vascularisation and mitosis of steroidogenic cells. These stage-specific mechanisms also may contribute to gain the function of prostaglandin F2 (PGF2 )-resistant CL at this stage. Recent studies suggest that the vasoactive peptide angiotensin II (Ang II) regulates luteal function. Thus, this study aimed to investigate (i) the expression of angiotensinconverting enzyme (ACE) mRNA by RT-PCR and the ACE protein expression by immunohistochemistry, (ii) the effects of angiogenic growth factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), on the secretion of Ang II, PGF2 , progesterone and oxytocin (OT), and (iii) the effects of luteal vasoactive peptides (Ang II and endothelin-1 (ET-1)) or OT on the secretion of PGF2 , progesterone and OT from bovine early CL (days 3-4 of the oestrous cycle), and evaluate a possible interaction of these substances with PGF2 . The expression of mRNA for ACE was found in theca interna of mature follicle, early CL and endothelial cells from developing CL as well as pituitary and kidney, but granulosa cells of mature follicle were negative. The immunohistochemical analysis revealed that blood capillaries (endothelial cells) were stained for ACE, but luteal cells were negative in early CL. To examine the effects of substances on the secretory function of the CL, an in vitro microdialysis system was used as a model. The infusion of bFGF and VEGF stimulated Ang II and PGF2 secretion as well as progesterone, but not OT secretion in early CL. The infusion of Ang II after PGF2 infusion continued the stimulatory effect on progesterone and OT release within early CL until 3 h thereafter. However, the infusion of ET-1 alone had no effect on progesterone or OT release. The infusion of luteal peptides such as Ang II and OT stimulated PGF2 secretion, whereas the infusion of ET-1 did not. In conclusion, the overall results of this study indicate that a functional angiotensin system exists on the endothelial cells of early CL, and that angiogenic factors bFGF and VEGF upregulate luteal Ang II and PGF2 secretion, which fundamentally supports the mechanism of progesterone secretion in bovine early CL. This idea supports the concept that the local regulatory mechanism involved in active angiogenesis ensures the progesterone secretion in the developing CL in vivo.

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“…Based on an in vitro study (Speroff & Ramwell 1970), a direct PGF steroidogenic stimulation of luteal cells has been suggested (Hixon & Hansel 1974). Direct inhibitory and stimulating effects of PGF on small and large luteal cells respectively have been demonstrated in vitro (Alila et al 1988, Meidan et al 1992, Girsh et al 1995, Okuda et al 1998, Skarzynski & Okuda 1999. In addition, the results of studies involving treatment with a bolus luteolytic dose of PGF have been interpreted to indicate that nitric oxide is a crucial factor in initiating luteolysis through a drastic increase in luteal blood flow (Shirasuna et al 2008), and that the induced increase in luteal blood flow is the first step in the luteolytic cascade (Miyamoto et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Luteal blood flow and concentrations of circulating progesterone and other hormones associated with a simulated pulse of 13,14-dihydro-15-keto-prostaglandin F2α in heifers

Shrestha¹,

Beg²,

Imam³

et al. 2010

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Progesterone and luteal blood flow effects of an i.u. 2-h infusion of 0.25 mg/h of prostaglandin F 2a (PGF) that simulated a natural pulse of 13,14-dihydro-15-keto-PGF (PGFM) were compared to the effects of a single bolus i.u. injection of PGF (4 mg) that induced complete luteolysis in heifers. Blood sampling and an estimate of the percentage of luteal area with colour-Doppler signals of blood flow were performed every 2 min for 20 min and less frequently thereafter for 6 h. After the beginning of PGF infusion or a bolus injection, progesterone increased to a peak at 14 and 10 min respectively, and was accompanied by an increase in blood flow in the bolus group but not in the infusion group. Progesterone then decreased for 1 or 2 h and was accompanied by a continued elevation in blood flow in the PGF bolus group and by a slight increase in the PGF infusion group. Progesterone then rebounded in both groups, but the rebound was greater in the infusion group. Blood flow decreased during the descending arm of the progesterone rebound. Cortisol and prolactin began to increase 6 min after the bolus PGF injection but did not increase during or after PGF infusion. The increases in cortisol, prolactin and blood flow after a PGF bolus treatment but not during a simulated PGFM pulse indicated that the bolus treatment was pharmacologic, and its use may lead to faulty conclusions on the nature of physiologic luteolysis. The comparisons between progesterone and blood flow are novel.

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Control of progesterone production in small and large bovine luteal cells separated by flow cytometry

Cited by 121 publications

References 26 publications

Localization of prostaglandin F2 inhibition of lipoprotein use by bovine luteal cells

Localization of prostaglandin F2 inhibition of lipoprotein use by bovine luteal cells

Production and localisation of angiotensin II in the bovine early corpus luteum: a possible interaction with luteal angiogenic factors and prostaglandin F2 alpha

Luteal blood flow and concentrations of circulating progesterone and other hormones associated with a simulated pulse of 13,14-dihydro-15-keto-prostaglandin F2α in heifers

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