Effect of 1,25-dihydroxyvitamin D3 on TSH secretion from rat pituitary cells in culture

Abstract. The effect of 1,25-dihydroxyvitamin D3 ( 1,25(OH)2D3) on TSH secretion from rat pituitary cells was studied. When incubating cells with 1,25(OH)2D3 even at 100 × the physiological concentrations (10−8), no effect on basal TSH secretion was observed. The TRH-induced TSH secretion increased after a 24-h incubation with 10−8 mol/l 1,25(OH)2D3 (2.9 ± 0.2 ng/well vs 4.3 ± 0.5 ng/well, mean ± sd; P < 0.05). When serum was omitted from the incubation medium, the potentiating effect of 1,25(OH)2D3 on the TRH-induced TSH release was blunted. No effect on cellular protein content was observed after incubating the cells with 10−8 mol/l 1,25(OH)2D3. The results indicate that at unphysiological concentrations, 1,25(OH)2D3 affects the TRH-induced TSH secretion from pituitary cells. The physiological significance remains unclear.

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Effects of tri-iodothyronine, cortisol and transcriptional inhibitors on vitamin D3-enhanced thyrotrophin secretion by rat pituitary cells in vitro

Journal of Endocrinology ◽

10.1677/joe.0.1210451 ◽

1989 ◽

Vol 121 (3) ◽

pp. 451-458 ◽

Cited By ~ 3

Author(s):

M. C. d'Emden ◽

J. D. Wark

Keyword(s):

Primary Cultures ◽

Relative Increase ◽

Pituitary Cells ◽

Dihydroxyvitamin D ◽

Rat Pituitary ◽

Tsh Secretion ◽

Dependent Inhibition ◽

Rat Pituitary Cells

ABSTRACT The hormone 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) has been shown to selectively enhance agonist-induced TSH release in the rat thyrotroph in vitro. The interaction of 1,25-(OH)2D3 with tri-iodothyronine (T3) and cortisol was studied in primary cultures of dispersed anterior pituitary cells. TRH (1 nmol/l)-induced TSH release over 1 h was enhanced by 70% (P<0·01) following exposure to 10 nmol 1,25-(OH)2D3/l for 24 h. Pretreatment with T3 (1 pmol/l–1 μmol/l) for 24 h caused a dose-dependent inhibition of TRH-induced TSH release. Net TRH-induced TSH release was inhibited by 85% at T3 concentrations of 3 nmol/l or greater. Co-incubation with 1,25-(OH)2D3 resulted in enhanced TRH-induced TSH release at all T3 concentrations tested (P<0·001). The increment of TRH-induced TSH release resulting from 1,25-(OH)2D3 pretreatment was equivalent in the presence or absence of maximal inhibitory T3 concentrations. At 1 nmol T3/1, there was a two- to threefold relative increase in 1,25-(OH)2D3-enhanced TRH-induced TSH release. Incubation with cortisol (100 pmol/l–100 nmol/l) had no effect on basal or TRH-induced TSH release, nor did it alter 1,25-(OH)2D3-enhanced TRH-induced TSH release when added 24 h before, or at the time of addition of 1,25-(OH)2D3. Actinomycin D and α-amanitin abolished 1,25-(OH)2D3-enhanced TSH secretion. These data demonstrate that the action of 1,25-(OH)2D3 in the thyrotroph required new RNA transcription, and was not affected by cortisol. In the presence of T3, the response of the thyrotroph to TRH induced by 1,25-(OH)2D3 was increased. We have shown that 1,25-(OH)2D3 has significant effects on the action of TRH and T3 in vitro. These findings support the proposal that 1,25-(OH)2D3 may modulate TSH secretion in vivo. Journal of Endocrinology (1989) 121, 451–458

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An acute release of Ca2+ from sequestered intracellular pools is not the primary transduction mechanism causing the initial burst of PRL and TSH secretion induced by TRH in normal rat pituitary cells

Cell Calcium ◽

10.1016/0143-4160(92)90045-t ◽

1992 ◽

Vol 13 (3) ◽

pp. 173-182 ◽

Cited By ~ 7

Author(s):

N. Sato ◽

X. Wang ◽

M.A. Greer

Keyword(s):

Pituitary Cells ◽

Initial Burst ◽

Transduction Mechanism ◽

Rat Pituitary ◽

Tsh Secretion ◽

Normal Rat ◽

Rat Pituitary Cells

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Dopaminergic control of TSH secretion in isolated rat pituitary cells

FEBS Letters ◽

10.1016/0014-5793(80)80356-5 ◽

1980 ◽

Vol 121 (2) ◽

pp. 257-259 ◽

Cited By ~ 15

Author(s):

Steven M. Foord ◽

John Peters ◽

Maurice F. Scanlon ◽

Bernard Rees Smith ◽

Reginald Hall

Keyword(s):

Pituitary Cells ◽

Rat Pituitary ◽

Tsh Secretion ◽

Rat Pituitary Cells ◽

Isolated Rat ◽

Dopaminergic Control

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Vitamin D-enhanced thyrotrophin release from rat pituitary cells: effects of Ca2+, dihydropyridines and ionomycin

Journal of Endocrinology ◽

10.1677/joe.0.1210441 ◽

1989 ◽

Vol 121 (3) ◽

pp. 441-450 ◽

Cited By ~ 6

Author(s):

M. C. d'Emden ◽

J. D. Wark

Keyword(s):

Vitamin D ◽

Pituitary Tumour ◽

Prolactin Secretion ◽

Pituitary Cells ◽

Dihydroxyvitamin D ◽

Normal Pituitary Gland ◽

Rat Pituitary ◽

Rat Pituitary Cells

ABSTRACT Vitamin D may regulate pituitary function, as there are selective effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on gene expression in clonal pituitary tumour cells, and on TRH-induced TSH release in normal rat pituitary cells in vitro. The role of Ca2+ in 1,25-(OH)2D3-enhanced TSH release from primary rat pituitary cell cultures was investigated. Pretreatment with 10 nmol 1,25-(OH)2D3/l for 24 h augmented KCl (3–60 mmol/l)-induced TSH release over 1 h at all KCl concentrations greater than 7·5 mmol/l (P< 0·001), with a 76% enhancement of TSH release induced by 30 mmol KCl/l (P<0·001). The Ca2+ channel antagonist nifedipine (10 nmol/l–10 μmol/l) caused a concentration-dependent inhibition of KCl (60 mmol/l)-induced TSH secretion. Pretreatment with 1,25-(OH)2D3 enhanced KCl-induced release at all concentrations of nifedipine (P<0·001). The Ca2+ selective divalent cation ionophore ionomycin (1 nmol/l–1 μmol/l), and the Ca2+ channel agonist BAY K 8644 (10 nmol/l–1 μmol/l) increased prolactin secretion but did not increase TSH release, and 1,25-(OH)2D3 had no effect. At an extracellular Ca2+ concentration of less than 500 nmol/l, TRH-induced TSH release was observed only after treatment with 1,25-(OH)2D3 (P<0·01). As the extracellular Ca2+ concentration was increased, greater increments of TRH-induced TSH release were observed following pretreatment with 1,25-(OH)2D3 (P<0·01). However, the effect of 1,25-(OH)2D3 in the thyrotroph was independent of the pretreatment extracellular Ca2+ concentration. We have shown that 1,25-(OH)2D3 acts selectively on the thyrotroph to enhance in-vitro responsiveness to TRH and KCl. These data suggest that the action of 1,25-(OH)2D3 in the thyrotroph is to enhance intracellular signal transduction. They further support a permissive or regulatory role of vitamin D in the normal pituitary gland. Journal of Endocrinology (1989) 121, 441–450

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Effect of 1,25-dihydroxyvitamin D3 on rat pituitary prolactin release

Acta Endocrinologica ◽

10.1530/acta.0.1160459 ◽

1987 ◽

Vol 116 (4) ◽

pp. 459-464 ◽

Cited By ~ 10

Author(s):

Kid Törnquist

Keyword(s):

Pituitary Cells ◽

Dihydroxyvitamin D3 ◽

Enhancing Effect ◽

Hydroxyvitamin D ◽

Dihydroxyvitamin D ◽

Rat Pituitary ◽

25 Hydroxyvitamin D ◽

Pituitary Prolactin

Abstract. The effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on PRL secretion from rat pituitary in vivo and in vitro was investigated. Treating the rats for three days with 0.05 μg/kg per day had no effect on basal PRL secretion, whereas the TRH-induced PRL secretion was increased (P < 0.001). The enhancing effect of 1,25(OH)2D3 was blunted by verapamil. Incubating dispersed anterior pituitary cells with 10−8 mol/l 1,25(OH)2D3 induced a significant increase in PRL secretion after 96 h (364 ± 30 ng/well vs 481 ± 33 ng/well, P < 0.001; mean ± sem) compared with control cells. The TRH-induced PRL secretion was increased in cells incubated with 1,25(OH)2D3 for 144 h (0.766 ± 0.061 vs 1.024 ± 0.076 μg/well, P < 0.05; mean ± sem) compared with control cells. Neither 25-hydroxyvitamin D3 (25OH-D3) nor 24,25-dihydroxyvitamin D3 had any effects on the PRL secretion. However, when the cells were incubated with both 10−8 mol/l 1,25(OH)2D3 and 10−6 mol/l 25OHD3, the enhancing effect of 1,25(OH)2D3 on the basal PRL secretion was blunted. The results suggest that 1,25(OH)2D3 possibly affects the regulation of PRL release from the rat pituitary and that this effect is specific for 1,25(OH)2D3.

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