Temporal Sequence of Prolactin Actions on Phospholipid Biosynthesis in Mouse Mammary Gland Explants*

Rillema, James A.; Foley, Karen A.; Etindi, Ransome N.

doi:10.1210/endo-116-2-511

Cited by 8 publications

(4 citation statements)

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“…PRL at physiological concentrations (50-1,000 ng/ml) functioned in concert with insulin and cortisol to stimulate phosphate uptake as well as its incorporation into lipids and TCA-insoluble materials. The onset of these PRL responses was 8-12 h after PRL addition to the cultured tissues; this correlates well with the onset of PRL's effect on the synthesis of a number of other milk products, including lactose, casein, and triglycerides; the PRL stimulation of iodide, amino acid, and glucose transport follows a similar time course (1,3,4,(6)(7)(8)(9)(10)(11). Precisely how all the signaling pathways for PRL, insulin, and cortisol integrate to effect a maximum stimulation of milk product synthesis remains to be explained.…”

Section: Discussionsupporting

confidence: 55%

Effect of prolactin on phosphate transport and incorporation in mouse mammary gland explants

Rillema

2002

American Journal of Physiology-Endocrinology and Metabolism

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Rillema, James A. Effect of prolactin on phosphate transport and incorporation in mouse mammary gland explants. Am J Physiol Endocrinol Metab 283: E132-E137, 2002. First published December 18, 2001 10.1152/ajpendo.0409.2001Inorganic phosphate is present in milk at a concentration that is severalfold higher than in maternal plasma. In cultured mammary tissues from 12-to 14-day-pregnant mice, the intracellular concentration of 32 PO4 was six times higher than in the culture medium after a 4-h treatment with 32 PO4. Of the principal lactogenic hormones [insulin (I), cortisol (H), and prolactin (PRL)], only I and PRL (in the presence of H and I) stimulated 32 PO4 uptake into cultured mammary tissues; H, by itself or in the presence of I or PRL, inhibited 32 PO4 uptake. All three lactogenic hormones together effected the greatest stimulation of 32 PO4 uptake. Similar hormone effects were observed with regard to 32 PO4 incorporation into lipids and trichloroacetic acid-insoluble molecules. In a time course study, the onset of the PRL stimulation of 32 PO4 uptake and incorporation occurred 8-12 h after PRL addition; in dose-response studies, the PRL effect was manifested with PRL concentrations of 50 ng/ml and above. From kinetic studies, the apparent maximal velocity of PO4 uptake was determined to be ϳ7.7 mM ⅐ h Ϫ1 ⅐ l cell water Ϫ1 ; the apparent Michaelis-Menten constant was ϳ3-5 mM. The PRL effect on 32 PO4 uptake was abolished when sodium was absent from the uptake medium. These studies thus demonstrate a complex interaction of three hormones (I, H, and PRL) in the regulation of 32 PO4 uptake and incorporation into macromolecules in cultured mouse mammary tissues.insulin; cortisol PHOSPHATE IS AN ESSENTIAL COMPONENT of milk for the nourishment of the neonate. In milk, it is present in several forms, including inorganic phosphate, colloidal phosphate, and casein phosphate and in phospholipids (5, 12). Because of the high concentration of phosphate in milk that meets the nutritional demands of the suckling neonate, copious amounts of phosphate are transferred from the maternal plasma into milk. One author (2) reported that all of the plasma inorganic phosphate is replaced every 10 min in lactating rats.Even when only inorganic phosphate is considered, its concentration in milk is 5-to 10-fold higher than in the maternal plasma. A highly efficient transport mechanism is therefore obviously present in the alveolar epithelial cells of the mammary gland. Shillingford et al. (13) recently characterized one phosphate transport mechanism in lactating rat mammary glands. Phosphate uptake was predominantly via a sodium-dependent transport mechanism, presumably located on the basolateral membrane of the alveolar epithelial cells; a sodium-phosphate symporter was postulated. Phosphate uptake occurred via a saturable mechanism with an apparent Michaelis-Menten constant (K m ) of 1.13 mM.The experiments reported in this study were carried out to characterize the effects of three lactogenic hormones [insulin, cortisol, and prol...

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Section: Discussionsupporting

confidence: 55%

Effect of prolactin on phosphate transport and incorporation in mouse mammary gland explants

Rillema

2002

American Journal of Physiology-Endocrinology and Metabolism

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“…The lactogenic activity of prolactin, growth hormone (GH) and placental lactogen (PL) has been demonstrated in numerous in-vivo and in-vitro studies (Cowie, Forsyth & Hart, 1980). Many of these studies have used heterologous systems in which mouse mammary tissue was employed as the target organ to analyse the lactogenic activity of prolactin, GH and PL from a wide variety of species (Rivera & Bern, 1961;Turkington & Topper, 1966;Forsyth & Parke, 1973;Vonderhaar, 1977; Ways, Markoff, Ogren & Talamantes, 1979;Ono, Perry & Oka, 1981;Rillema, Foley & Etindi, 1985;Rocha, Ringo & Read, 1985). On the other hand, only a few studies have described the lactogenic response of mouse mammary tissue to prolactin-like hormones from the mouse.…”

Section: Introductionmentioning

confidence: 99%

Lactogenic response of cultured mouse mammary epithelial cells to mouse placental lactogen

Thórdarson¹,

Villalobos²,

Colosi³

et al. 1986

Journal of Endocrinology

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The ability of mouse placental lactogen (mPL), mouse prolactin (mPRL), mouse GH (mGH) and ovine prolactin (oPRL) to stimulate synthesis of alpha-lactalbumin was tested in a primary culture of mouse mammary gland epithelial cells. Mammary tissue was obtained from 10-day pregnant Swiss Webster mice, enzymatically dissociated and the cells were cultured on floating collagen gels for 5 days. The basic culture medium consisted of Nutrient Mixture F12/Dulbecco's Modified Eagle's Medium (1:1, v/v), containing 10 mg insulin/1, 5 mg cortisol/l, 10 micrograms epidermal growth factor/l, 5 g bovine serum albumin/l and 50 mg gentamycin/l. Mouse PL, mPRL, mGH and oPRL were added to the basic medium in concentrations from 1 microgram/l to 1 mg/l. Accumulation of alpha-lactalbumin in the culture medium was measured. For that purpose, mouse alpha-lactalbumin was purified from mammary tissue obtained from lactating Swiss Webster mice and a radioimmunoassay was developed. Mouse PL, mPRL and oPRL stimulated a dose-dependent increase in alpha-lactalbumin secretion. Mouse GH also caused a significant, but dose-independent, increase in alpha-lactalbumin secretion. Mouse PL showed the greatest activity in stimulating alpha-lactalbumin secretion. It was concluded that mPL is an important lactogenic hormone in the latter half of pregnancy in the mouse, when circulating mPRL concentrations are low.

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“…PRL also had no early (0-12 hour) effect on the incorporation of [ 32 P]04, [ 3 H]-choline, [ 3 H]-ethanolamine, or [ 3 H]-inositol (Rillema, Foley and Etindi 1985) incorporation into specific phospholipid fractions, although effects of PRL on the incorporation of all these substrates were observed when culture periods with PRL of 12 hours or more were used. Although the onset of a PRL stimulation of [ H]-serine incorporation into organic-soluble materials occurred a bit earlier (8 hours), this effect is relatively small (16% increase) and is accompanied by an enhanced rate of transport of [ H ]-serine into the cells.…”

Section: Discussionmentioning

confidence: 95%

Sequence of Prolactin Effects on Phospholipid Synthesis in Mouse Mammary Gland Explants

Rillema¹,

Waters²,

Whale³

1990

Horm Metab Res

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In cultured mouse mammary gland explants derived from 12-14 day pregnant mice, the effect of prolactin (PRL) on the rate of incorporation of several precursors into neutral lipids and phospholipids was determined. Employing [14C]-acetate as a substrate, PRL stimulates its incorporation into a) neutral lipids by 4-6 hours, b) phosphatidyl choline (PC) and phosphatidyl inositol-phosphatidyl serine (PI-PS) by 1-2 hours, and c) phosphatidyl ethanolamine (PE) by 2-4 hours. Using [3H]-glycerol as a substrate, the temporal response to PRL for its incorporation into the neutral lipids was the same as that for [14C]-acetate, however, PRL did not enhance the rate of [3H]-glycerol incorporation into the phospholipids at any time through 16 hours. PRL similarly had no effect on the rates of [3H]-choline, [3H]-serine, [3H]-ethanolamine, or [32P]O4 incorporation into the phospholipids at hormone exposure periods of 8 hours or more. And finally, PRL had no effect on the rates of [3H]-arachidonate or [14C]-linoleate incorporation into neutral lipids or phospholipids at culture periods up to 18 hours. These data suggest that the early effect of PRL on [14C]-acetate incorporation into the phospholipids is due to either the insertion of newly synthesized fatty acids and/or the extension of fatty acids contained in the phospholipids.

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Temporal Sequence of Prolactin Actions on Phospholipid Biosynthesis in Mouse Mammary Gland Explants*

Cited by 8 publications

References 8 publications

Effect of prolactin on phosphate transport and incorporation in mouse mammary gland explants

Effect of prolactin on phosphate transport and incorporation in mouse mammary gland explants

Lactogenic response of cultured mouse mammary epithelial cells to mouse placental lactogen

Sequence of Prolactin Effects on Phospholipid Synthesis in Mouse Mammary Gland Explants

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