High density lipoprotein uptake and utilization by rat corpora lutea: the effects of prolactin and prostaglandin F2a

Rajkumar, K.; Couture, Roxanne; Murphy, Bruce D.

doi:10.1016/0022-4731(84)90727-1

Cited by 5 publications

(5 citation statements)

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“…The addition of serum increased overall progesterone production, probably due to an availability of lipoprotein for steroidogenesis [6,[33][34][35][36] and to stimulation of cellular activity, as serum contains hormones and/or inhibitors of hormonal action. Similar results have been obtained from the culture of bovine [37], human [38], ovine [39], rat [40], and monkey [41] luteal cells. The responses observed in incubates containing calf serum in our study were not identical among the groups (interaction effects) and could be due to species incompatibility.…”

Section: Discussionsupporting

confidence: 87%

Evaluation of in Vitro Culture Conditions to Demonstrate Pregnancy-Dependent Changes in Luteal Function in the Pig1

Więsak

Hardin

Foxcroft

1994

Biology of Reproduction

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This study was designed to evaluate the most effective in vitro culture conditions for study of pregnancy-dependent changes in LH-stimulated steroidogenesis in porcine luteal tissue. Mixed luteal cells recovered from the CL of cyclic (Day 12) and pregnant (Day 12 and 16) pigs were incubated either in Eagle's minimum essential medium (MEM) or in MEM supplemented with different concentrations of porcine or calf serum or BSA, or were incubated in a defined medium (DM) containing 2 micrograms/ml insulin, 40 ng/ml hydrocortisone, 5 micrograms/ml transferrin, and 10(-7) M thyroxine. Cultures were treated with various doses of porcine LH (0.1, 1, 10, 100 ng/ml). Additionally, large and small luteal cells of Day 12 cyclic and pregnant pigs were incubated for 4 h in medium 199 supplemented with 2% porcine serum in the absence or presence of various concentrations of LH. Overall, progesterone production by the luteal cells of Day 12 pregnant pigs was significantly (p < 0.05) higher than that by cells of the cyclic pigs. However, the luteal cells of pregnant Day 16 pigs released significantly (p < 0.05) less progesterone than the other groups. LH had a stimulatory effect (p < 0.001) on progesterone release by mixed luteal cells that was independent of the type of medium supplementation or reproductive status. Porcine serum, calf serum, and BSA (p < 0.001, p < 0.001, and p < 0.05, respectively) also stimulated progesterone production. However, the doses of porcine and calf serum or BSA that stimulated progesterone release were dependent on the reproductive status of the pig.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 87%

Evaluation of in Vitro Culture Conditions to Demonstrate Pregnancy-Dependent Changes in Luteal Function in the Pig1

Więsak

Hardin

Foxcroft

1994

Biology of Reproduction

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“…The 25-hydroxycholesterol readily diffuses into the mitochondria, to the site of cholesterol side-chain cleavage, and can be used as an indicator of side-chain cleavage activity (Toaff et al, 1982). The increase in progesterone production in response to 25-hydroxycholesterol treatment in the present study is consistent with results obtained in rat (Rajkumar et al, 1985(Rajkumar et al, , 1988, hamster (Silavin & Strauss, 1983) and rabbit luteal cells (McLean et al, 1987), as well as in rat luteal mitochondria (Toaff et al, 1982). The very large stimulation of steroidogenesis by 25-hydroxycholesterol in this study was expected since these cells had been deprived of cholesterol substrate for five days in serum-free culture.…”

Section: Cellular Uptake Of Lipoprotein-carried Cholesterolsupporting

confidence: 91%

“…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%

“…PGF2u has been shown to suppress luteinizing hormone (LH)-stimulated, 3',5'-cyclic adenosine monophosphate (cAMP)-stimulated (Jordan, 1981;Pate & Condon, 1984;Benhaim et al, 1987) and lipoprotein-stimulated (Pate & Nephew, 1988;Pate & Condon, 1989) progesterone produc¬ tion. However, PGF-,U has no effect on low-density lipoprotein (LDL) or high-density lipoprotein (HDL) uptake in bovine luteal cells (Pate & Condon, 1989), or on HDL binding (Rajkumar et al, 1985) or LDL binding (Rajkumar et al, 1988) in rat luteal cells, and thus PGF2a may allow uptake of lipoprotein-carried cholesterol into the cell but inhibit the subsequent use of cholesterol for steroidogenesis.…”

Section: Introductionmentioning

confidence: 99%

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

Grusenmeyer¹,

Pate²

1992

Reproduction

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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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“…In vivo, PGF 2␣ decreased luteal concentrations of mRNA encoding LDL-R (312, 360) but increased mRNA for HDL-BP in ewes (360). In addition, treatment of rats with PGF 2␣ did not decrease HDL uptake (295). Because ovine luteal cells preferentially utilize HDL for a cholesterol source (387) and suppression of LDL-R mRNA did not decrease concentrations of progesterone in serum (T. Tandeski, J. Juengel, and G. Niswender, unpublished observations), it does not seem likely that decreased uptake of lipoprotein occurs after PGF 2␣ treatment in vivo.…”

Section: Effect Of Pgf 2␣ On Uptake Of Lipoprotein and Release Of Chomentioning

confidence: 95%

Mechanisms Controlling the Function and Life Span of the Corpus Luteum

Niswender

Juengel

Silva

et al. 2000

Physiological Reviews

854

553

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The primary function of the corpus luteum is secretion of the hormone progesterone, which is required for maintenance of normal pregnancy in mammals. The corpus luteum develops from residual follicular granulosal and thecal cells after ovulation. Luteinizing hormone (LH) from the anterior pituitary is important for normal development and function of the corpus luteum in most mammals, although growth hormone, prolactin, and estradiol also play a role in several species. The mature corpus luteum is composed of at least two steroidogenic cell types based on morphological and biochemical criteria and on the follicular source of origin. Small luteal cells appear to be of thecal cell origin and respond to LH with increased secretion of progesterone. LH directly stimulates the secretion of progesterone from small luteal cells via activation of the protein kinase A second messenger pathway. Large luteal cells are of granulosal cell origin and contain receptors for PGF(2alpha) and appear to mediate the luteolytic actions of this hormone. If pregnancy does not occur, the corpus luteum must regress to allow follicular growth and ovulation and the reproductive cycle begins again. Luteal regression is initiated by PGF(2alpha) of uterine origin in most subprimate species. The role played by PGF(2alpha) in primates remains controversial. In primates, if PGF(2alpha) plays a role in luteolysis, it appears to be of ovarian origin. The antisteroidogenic effects of PGF(2alpha) appear to be mediated by the protein kinase C second messenger pathway, whereas loss of luteal cells appears to follow an influx of calcium, activation of endonucleases, and an apoptotic form of cell death. If the female becomes pregnant, continued secretion of progesterone from the corpus luteum is required to provide an appropriate uterine environment for maintenance of pregnancy. The mechanisms whereby the pregnant uterus signals the corpus luteum that a conceptus is present varies from secretion of a chorionic gonadotropin (primates and equids), to secretion of an antiluteolytic factor (domestic ruminants), and to a neuroendocrine reflex arc that modifies the secretory patterns of hormones from the anterior pituitary (most rodents).

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High density lipoprotein uptake and utilization by rat corpora lutea: the effects of prolactin and prostaglandin F2a

Cited by 5 publications

References 0 publications

Evaluation of in Vitro Culture Conditions to Demonstrate Pregnancy-Dependent Changes in Luteal Function in the Pig1

Evaluation of in Vitro Culture Conditions to Demonstrate Pregnancy-Dependent Changes in Luteal Function in the Pig1

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

Mechanisms Controlling the Function and Life Span of the Corpus Luteum

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