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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of oophorectomy on the biological indices of bone remodelling and the time-course of their changes are described. In the first few months following surgical menopause the measurement of the markers of bone remodelling indicates that the increase in osteogenesis is delayed compared with that of bone resorption; this prevalence of destruction over new bone deposition justifies the deficiency of skeletal balance, shortly after acute oestrogen deficiency. The changes in bone remodelling are accompanied by an increase in serum calcium while serum immunoreactive parathyroid hormone levels remain unchanged or even decrease, suggesting a shift to right of the parathyroid gland set-point. The reasons for the negative skeletal balance after oophorectomy might be sought therefore at bone tissue level, even if changes in responsiveness and/or of the parathyroid gland set-point could also be contributory.
J Steroid Biochem Mol Biol 1990 Nov 20
PMID:The effects of oophorectomy on skeletal metabolism. 225 50

We have demonstrated previously that 17 beta-estradiol (E2) stimulates cell proliferation in skeletal tissues, as measured by increased DNA synthesis and creatine kinase (CK) specific activity, and that calciotrophic hormones modulate E2 activity in rat osteoblastic sarcoma cells (ROS 17/2.8). Moreover, E2 failed to stimulate DNA synthesis in vitamin D-depleted female rat bone in the absence of prior i.p. injections of 1.25(OH)2D3. We have, therefore, studied the effects of pretreatment of cells by one hormone on their response to challenge by a second hormone. We now report reciprocal interactions of sex steroids and other hormones modulating bone formation on cell proliferation parameters in primary bone and cartilage cell cultures: these interactions can selectively augment or diminish cell responsiveness to a given hormone. Pretreatment of rat epiphyseal cartilage cell cultures with 1.25(OH)2D3, 24.25(OH)2D3 or parathyroid hormone (PTH) for 5 days, followed by E2 treatment for 24h, resulted in increased DNA synthesis compared to cultures pretreated with vehicle. Prostaglandin (PGE2) pretreatment blocked further response to E2. In the reciprocal case, rat epiphyseal cartilage cells, pretreated with E2, showed an increased response to PTH, a loss of the response to PGE2 or 24.25(OH)2D3 and an inhibition of CK activity and DNA synthesis by 1.25(OH)2D3, similar to the characteristic inhibitory action of 1.25(OH)2D3 in osteoblasts. By contrast, rat epiphyseal cartilage cells pretreated with testosterone showed no changes in response to PTH, 24.25(OH)2D3 or PGE2 and a decreased response to E2, but were stimulated by 1.25(OH)2D3. Rat embryo calvaria cell cultures behaved similarly to epiphyseal cartilage cultures except that 24.25(OH)2D3 pretreatment did not increase the response to E2. Reciprocally, pretreatment with E2 before exposure to calciotrophic hormones did not change the responses of rat embryo calvaria cell cultures to 1.25(OH)2D3 or 24.25(OH)2D3. These findings suggest that the mutual interactions between calciotrophic hormones and E2, demonstrated here in vitro, could selectively affect the responses of bone and cartilage cells to E2 by several mechanisms. These possibilities include increased E2 receptors and E2-stimulated differentiation of cartilage cells to more E2 responsive cells showing some characteristics of osteoblasts.
J Steroid Biochem Mol Biol 1990 Nov 30
PMID:Reciprocal modulation by sex steroid and calciotrophic hormones of skeletal cell proliferation. 227 32

Parathyroid hormone-related peptide (PTHrP) has been detected in fetal serum and amniotic fluid. Using a combination of immunocytochemistry and molecular biology we have detected the peptide and its mRNA in a variety of fetal tissues throughout gestation. Tissue-specific mRNA isoforms were observed, the pattern of hybridization of which changed throughout gestation. In addition, the intensity and pattern of immunocytochemical localization of the peptide was found to vary over the time-period studied (8-30 weeks). PTHrP is expressed by a variety of tumours associated with the syndrome of humoral hypercalcaemia of malignancy and probably accounts for the hypercalcaemia by virtue of its limited amino acid homology with parathyroid hormone. These data demonstrate for the first time that PTHrP, a tumour-related peptide, is expressed during normal human fetal development, and suggest the possibility that it may function to regulate fetal calcium balance and growth in utero.
J Mol Endocrinol 1990 Dec
PMID:Parathyroid hormone-related peptide in normal human fetal development. 228 37

Several pentapeptides included in the 44-68 sequence of human parathyroid hormone (hPTH) were synthesized simultaneously on benzhydrylamine and m-nitrobenzhydrylamine resins. The first polymer gave the free peptide and the second the peptidyl-resin complex. An ELISA test carried out with each peptidyl-resin complex showed that all the anti-44-68 hPTH antibodies raised in different animal species are directed against the same hPTH pentapeptidic sequence. This sequence is very hydrophilic and is specific to the hormone. This study demonstrates the importance of specific peptide chains in an epitope.
Mol Immunol 1985 Jun
PMID:Epitopes of the 44-68 human parathyroid hormone fragments: the importance of specific hydrophilic peptide sequences. 241 Jul 81

This report describes a series of studies on the regulation of teleocalcin secretion by primary cultures of rainbow trout corpuscles of Stannius, endocrine glands believed to be unique to bony fishes. Teleocalcin release by these cultured cells was stimulated specifically by calcium in a dose-related fashion. Magnesium did not mimic the effects of added calcium and varying the osmotic pressure had no effect on hormone release. The addition of either ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) or cobalt chloride blocked the stimulatory effects of added calcium, whereas the calcium ionophore A23187 mimicked the effects of calcium on hormone release. Mammalian and piscine pituitary hormones (prolactin, growth hormone and gonadotrophic hormone) had no effect on teleocalcin secretion. Inconclusive results were obtained with the calcium channel blockers, verapamil and nifedipine. The results are discussed in relation to calcium-regulated secretion of calcitonin and parathyroid hormone, as well as the known physiological effects of teleocalcin in fish.
Mol Cell Endocrinol 1989 Mar
PMID:Primary culture of teleocalcin cells from rainbow trout corpuscles of Stannius: regulation of teleocalcin secretion by calcium. 250 Nov 23

The extensive chromatographic characterization of four parathyroid hormone (PTH)-like proteins in a human bronchial carcinoid tumour associated with humoral hypercalcaemia and severe osteitis fibrosa is described. PTH-like bioactivity was detected in acetic acid extracts of the tumour using an in-vitro osteo-sarcoma cell bioassay. The active tumour proteins were positively charged at physiological pH and had apparent Mr of approximately 29,000, 16,000, 4000-9000 and less than 4000. The proteins were immunologically distinct from PTH, but each stimulated PTH-sensitive adenylate cyclase in cultured osteoblastic cells. There was no evidence of PTH gene expression by the tumour. These proteins represent different molecular forms of PTH-related protein.
J Mol Endocrinol 1989 Jan
PMID:Multiple forms of parathyroid hormone-like proteins in a human tumour. 254 21

Cardiovascular effects of parathyroid hormone (PTH) have been recently described. Pharmacological doses of PTH both reduce arterial pressure and increase blood flow of vascular beds. Two possible cellular mechanisms were investigated: (a) transmembrane Ca2+ fluxes and (b) cyclic AMP response in vascular smooth muscle. In vivo, results in the rat show that injection of synthetic bovine 1-34 fragment of PTH (bPTH-(1-34] produced a rapid (1-2 min) but transient (5-16 min) hypotensive effect which was dose-related (0.4-4 nmol.kg-1). In the in vitro studies on isolated rat aorta, bPTH-(1-34) partially inhibited noradrenaline (NA)-induced contractions by decreasing the sustained tonic component dependent on extracellular Ca2+. bPTH-(1-34) also produced relaxation of aorta preconstricted with NA or prostaglandin F2 alpha. Measurements of the lanthanum-resistant Ca2+ pool using 45Ca2+ showed that bPTH-(1-34) decreased basal Ca2+ uptake and partially inhibited Ca2+ uptake stimulated by NA or K+-depolarizing solution in a concentration-dependent fashion. In addition, bPTH-(1-34) caused a concentration-related increase in cyclic AMP in rat isolated aortic tissues. Hypotensive and vasorelaxing effects of bPTH-(1-34) thus appear to be mediated by a decrease in the amount of Ca2+ available for contraction and by an increase in cyclic AMP response in vascular smooth muscle cells.
Mol Cell Endocrinol 1989 Nov
PMID:Parathyroid hormone acute vascular effect is mediated by decreased Ca2+ uptake and enhanced cAMP level. 255 30

Proteins from bovine kidney membranes were separated by denaturating polyacrylamide gel electrophoresis and blotted onto nitrocellulose paper. The blots were immunostained with parathyroid hormone (PTH) antisera, and the effect of the presence of PTH on immunostaining was determined. Immunostaining of membrane proteins by two specific antisera was altered by PTH. With one antiserum, the immunostaining of two specific proteins (apparent mass 90 and 105 kDa) was prevented by PTH. With the second antiserum the immunostaining of a 150 kDa protein was prevented by the hormone. These effects were strongest with the 90 and 150 kDa proteins and these were investigated further. Antibody binding was prevented either by co-incubation or by preincubation of the blots with PTH, followed by washing and subsequent exposure to the antisera. Concentrations of PTH as low as 1 nM prevented antibody binding to the 90 kDa species, but somewhat higher PTH concentrations were required with the 150 kDa protein. Oxidation of the PTH methionine residues in the amino terminal segment of PTH, and deletion of the first nine residues in the hormone greatly reduced the competition with the 90 kDa protein, but had no effect on immunostaining of the 150 kDa species. The 35-84 fragment of PTH was not a competitor for the 90 kDa species, while the 1-34 fragment was ineffective with the 150 kDa protein.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Endocrinol 1989 Dec
PMID:Examination of parathyroid hormone antisera for the presence of receptor antibodies. 255 34

Parathyroid hormone-related protein (PTHrP), the peptide associated with humoral hypercalcemia of malignancy, has been identified in fetal and adult parathyroid glands. We here report a sub-clone of a rat parathyroid cell line which secretes a single peptide species corresponding in size to PTHrP(1-84). Biological activity of the secretion product was blocked by a specific antiserum against PTHrP, but not by parathyroid hormone (PTH) antiserum. Secretion of PTHrP by these cells was regulated by extracellular calcium in the physiological range. A single messenger RNA species for PTHrP was identified, though PTH mRNA could not be shown in these cells. Hybrid CAT genes containing 700-1000 bp of 5'-flanking DNA from the human PTH or PTHrP genes were transfected into these cells, and the PTHrP gene was expressed at 10-fold higher levels than the PTH gene. These cells thus provide a valuable model system for investigation expression of PTHrP in a non-transformed cell line.
Mol Cell Endocrinol 1989 Nov
PMID:Production of parathyroid hormone-related protein by a rat parathyroid cell line. 261 35

Previous in vitro studies concerning the renal metabolism of 25-hydroxyvitamin D3 (25(OH)D3) to form 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and 24,25R-dihydroxyvitamin D3 (24,25(OH)2D3) have utilized intact cell systems. In reflecting upon the possible mechanisms by which hormonally induced changes in the production of 1,25(OH)2D3 and 24,25(OH)2D3 may be brought about, we asked whether altered mitochondrial hydroxylase activities can quantitatively account for changes in the total cellular output of these steroids. Our objective was to delineate between extramitochondrial processes (e.g. altered substrate delivery), and those events restricted to the renal mitochondria (altered hydroxylase activities). We have examined the effect of pretreating primary cultures of chick kidney cells with either 1,25(OH)2D3 or parathyroid hormone (PTH) on 25(OH)D3-hydroxylase activities present in subsequently isolated mitochondria. Pretreatment with 10(-7) M 1,25(OH)2D3 reduced 1 alpha-hydroxylase activity in both cells and mitochondria to approximately 60% of control values by 1 h, and to 25-30% by 2 h. The effect of PTH (10 ng/ml) in both mitochondrial and whole cell preparations was an approximate 40% increase in measured 1 alpha-hydroxylase activity. 10 microM forskolin (FSK) elicited an approximate 2-fold increase in 1,25(OH)2D3 production. Reciprocal effects were observed with respect to 24-hydroxylase activity in both whole cell and mitochondrial preparations in response to exogenous 1,25(OH)2D3, PTH, and FSK. The findings demonstrate that these hormones initiate intracellular events which lead directly to altered 25(OH)D3 1 alpha- and 24-hydroxylase activities within the renal mitochondria.
Mol Cell Endocrinol 1989 Jun
PMID:25-Hydroxyvitamin D3 metabolism in mitochondria from primary renal cultures. 275 41


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