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Characterization of fully active biotinylated parathyroid hormone analogs. Application to fluorescence-activated cell sorting of parathyroid hormone receptor bearing cells.

[Nle8,18,Tyr34]bPTH-(1-34)amide (NlePTH) was biotinylated using sulfosuccinimidyl 6-(biotinamido)hexanoate, in dimethyl sulfoxide, and the multiple resulting peptides peaks were separated by reverse-phase high performance liquid chromatography. Their biological activities were compared with those of NlePTH, the parent compound, in radioreceptor and cAMP accumulation bioassays using rat osteosarcoma 17/2.8 cells; the earliest two eluting products, bioPTH 1 and 2, were equipotent, a third, bioPTH 3, was only 10% as potent, and the remaining, later eluting derivatives all were less than 0.1% as active. Competitive avidin binding assays using [3H]biotin suggested that bioPTH 1 and 2 had a single biotin congener per molecule, while bioPTH 3 contained two biotin residues. Upon Edman degradation, bioPTH 1 contained biotin on the lysine at position 13 of NlePTH; bioPTH 2's biotin was on the lysine at position 26 (or 27) and bioPTH 3 had biotins on lysines at both positions 13 and 26 (or 27). Avidin tagged with 125I, peroxidase, or fluorescein isothiocyanate was detected on bone-derived cells which had been incubated initially with bioPTH 2 (1, 10, and 100 nM) for 4 h, but not when NlePTH (1 microM) was added with bioPTH 2. A fluorescence-activated cell sorter detected a symmetrical shift in fluorescence of bone-derived cells incubated with 10 nM of bioPTH 2 and 10 micrograms/ml fluorescein isothiocyanate-avidin. Addition of a 30-fold molar excess of NlePTH, or omission of bioPTH 2, completely reversed this fluorescence shift, and no shift in fluorescence was seen with cells lacking PTH receptors. This fully active, high affinity biotinylated PTH-derivative should prove useful in the study of PTH receptor-bearing cells.

Animals

Intraoperative fall in plasma levels of intact parathyroid hormone in patients undergoing parathyroid adenomectomy.

Intraoperative measurement of intact parathyroid hormone (PTH) can be used to evaluate the success of parathyroid surgery in primary hyperparathyroidism associated with parathyroid adenoma. To evaluate this approach we used a modified immunoradiometric assay (IRMA) to study the kinetic patterns of circulating PTH disappearance in 13 patients undergoing adenomectomy for single adenoma. The rapid and the standard assay for PTH measurement in plasma were used and compared. The two methods showed a highly significant correlation (r = 0.995; p < 0.0001). We reported a decrease in PTH to 18.2 +/- 2.30 (mean +/- SEM) from baseline values at 15 minutes after successful parathyroid adenomectomy in the 13 patients. The biphasic pattern of serum PTH clearance was calculated in 8 of the studied patients with a fast phase showing a half-life (T1/2) of 3.99 (SEM 0.464) minutes and a slow phase with a T1/2 of 91.0 (SEM 33.6) minutes. Half the amount of the basal values was reached between 4 and 9 minutes. Our study concludes that the modified IRMA for intraoperative measurement is feasible, reliable and sufficiently precise for low hormone values. Since it may yield information on the half-life of PTH in the circulation, it may play a role in the surgical guidance for total exeresis of hyperfunctioning tissue.

Adenoma

Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro.

The effects of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2-16 h. There was a gradual suppression of PTH release (5-55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.

24,25-Dihydroxyvitamin D 3

The arterio-venous difference for immunoreactive parathyroid hormone and the production of adenosine 3,'5'-monophosphate by isolated perfused bone: studies with analogs of parathyroid hormone.

Recent studies suggest that the uptake of immunoreactive parathyroid hormone (iPTH) displays different characteristics in liver, kidney, and bone. Using the isolated perfused canine bone, we have characterized the uptake of two synthetic analogs of PTH, bovine PTH-(3-34) [bPTH-3(3-34)] and [Nle8,Nle18,Tyr34]bPTH-(3-34) amide, which had previously been shown to inhibit PTH-stimulated adenylate cyclase activity in renal membranes. During the infusion of synthetic bPTH-(1-34) (3 ng/ml), extraction of iPTH by isolated perfused bone averaged 37 +/- 1%, and cAMP production rose from 6.2 +/- 2.0 to 21 +/- 3 pmol/min. Extraction of bPTH-(3-34) was similar (35 +/- 2%), but cAMP levels did not increase over baseline with PTH concentrations as high as 100 ng/ml. Simultaneous infusion of bPTH-(1-34) and bPTH-(3-34) at molar ratios of 1:2 led to a 50% inhibition of PTH-stimulated cAMP increases. The extraction by bone of the more potent in vitro inhibitor of renal cortical adenylate cyclase [Nle8,Nle18,Tyr34]bPTH-(3-34) NH2 (3 ng/ml) averaged 39 +/- 2%. In contrast, cAMP production rose from a baseline of 5.6 +/- 0.5 to 12.5 +/- 2.0 pmol/min, demonstrating agonist activity for the analog. These studies show that [Nle3,Nle18,Tyr34]bPTH-(3-34) NH2 has agonist properties in isolated perfused bone, and unsubstituted bPTh-(3-34) inhibits PTH-stimulated cAMP release by perfused bone.

Animals

Secretion of parathyroid hormone by abnormal human parathyroid glands in vitro.

The secretory response of abnormal parathyroid glands obtained surgically from eleven patients with primary and secondary hyperparathyroidsm was tested in vitro. Short term flask studies were used to measure release of parathyroid hormone (PTH) at high (3.0 mM) and low (0.5 mM) calcium. Of eight adenomas, all but one showed increased release of hormone when exposed to low calcium ("responsive to calcium"), the degree of stimulation at three hours ranging from 15 to 209%. By comparison, two normal human glands were stimulated an average of 180%. Glands from three patients with secondary hyperplasia were also responsive to calcium. Thus, parathyroid glands from patients with primary and secondary hyperparathyroidism were characterized by a spectrum of responsiveness to calcium, and absolute "autonomy" was unusual. Even at high calcium concentrations, hormone release persisted at a low but definite level ("basal secretion"). The total number of functioning parathyroid cells is therefore a principal determinant in the oversecretion of PTH in hyperparathyroidism.

Adenoma

[Immunoreactive parathyroid hormones in the circulation and cerebrospinal fluid from patients with renal failure: possible restriction of parathyroid hormone by the blood-brain barrier].

There are reports that patients with renal failure have elevated circulating concentrations of parathyroid hormone (PTH), which is suspected to be a causal factor of the cerebral symptoms of these patients. A positive correlation between the circulating level of immunoreactive PTH and the extent of abnormality in the electroencephalogram (EEG) in humans has been reported. Moreover, in uremic dogs normalization of the EEG was observed after parathyroidectomy, and increased abnormality of the EEG was observed on infusion of PTH. If PTH is really a causal factor of uremic encephalopathy and abnormality of the EEG in patients with renal failure, the question arises as to whether PTH acts on the brain after penetrating through the blood-brain barrier or in some other way. In this work, we measured PTH by both C-terminal-specific RIA (C-PTH) and N-terminal-specific RIA (N-PTH) in the circulation and cerebrospinal fluid (CSF) of normal subjects and patients with renal failure. Blood and CSF samples were obtained from 7 normal volunteers (31 approximately 81 years old: 4 males and 3 females) and 22 patients with chronic renal failure (25 approximately 87 years old: 12 males and 10 females). No patients had a psychotic disease or endocrinopathy other than secondary hyperparathyroidism. Samples of venous blood were collected from the subjects after an overnight fast at the time of lumbar puncture for CSF sampling. C-terminal-specific RIA for measurement of the plasma and CSF concentrations of C-PTH was carried out using a commercially available RIA kit (Eiken Laboratory Inc., Tokyo, Japan).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Immunocytological evidence for parathyroid hormone in human fetal parathyroid glands.

Immunostaining with antiserum to bovine parathyroid hormone (PTH) was used to delineate the immunoreactive PTH (iPTH)-containing cells of parathyroid glands from 1 anencephalic and 29 normal human fetuses. The antiserum (GPO 3) cross-reacted with human PTH and recognized the carboxyl-terminal fragments of the PTH molecule. No iPTH-containing cells were observed in the parathyroid glands of the 6 fetuses younger than 10 weeks, in spite of the fact that organized parathyroid glands were identified by histological methods. By contrast, iPTH-containing cells were observed in all fetuses older than 10 weeks of gestation, including the anencephalic fetus. All cells were immunoreactive either at the cellular periphery or as a more diffuse cytoplasmic staining around the nucleus. No immunoreactive cells were observed in the thyroid or thymic parenchyma. The specificity of the immunocytological reaction was tested by the usual procedures. Previous in vitro studies suggested that parathyroid function might be active at 12 weeks of gestation. Our data suggest that iPTH is synthetized by parathyroid glands as as early as 10 weeks of gestation and is also present in the anencephalic fetus. The physiological significance of the early presence of PTH within the fetal parathyroid glands remains to be established.

Female

Dual effects of a new hypocalcemic agent, WR-2721, on cytoplasmic Ca2+ and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism.

The effects of the new hypocalcemic agent, WR-2721, on calcium-regulated parathyroid hormone (PTH) release, cytoplasmic Ca2+ (Ca2+i) and membrane potential were measured in dispersed parathyroid cells from patients with hyperparathyrodisim (HPT). The drug had no effects in the absence of extracellular Ca2+ but acted synergistically with Ca2+ in the 0.5-1.5 mM range by depolarizing the cells, increasing Ca2+i and inhibiting PTH release. Although the depolarizing effect of 3.0 mM Ca2+ was unaffected by WR-2721 the drug antagonized the effect of Ca2+ by decreasing Ca2+i and stimulating PTH release. Whereas the inhibitory actions of WR-2721 on PTH release may result from the activation of the mechanism for Ca2+ gating in the parathyroid cell plasma membrane, the stimulatory effect probably reflects increased intracellular Ca2+ sequestration. The drug is considered potentially important for the treatment of HPT.

Amifostine

Prolactin stimulation of parathyroid hormone secretion in bovine parathyroid cells.

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.

Adrenergic beta-Agonists