Even if the carboxyl-terminal (C-) fragments/intact (I-) PTH ratio is tightly regulated by the ionized calcium (Ca2+) concentration in humans and animals, in health and in disease, the physiological roles of C-PTH fragments and of the C-PTH receptor remain elusive. To explore these issues, we studied the influence of synthetic C-PTH peptides of various lengths on Ca2+ concentration and on the calcemic response to human (h) PTH-(1–34) and hPTH-(1–84) in anesthetized thyroparathyroidectomized (TPTX) rats. We also looked at the capacity of these PTH preparations to react with the PTH/PTHrP receptor and with a receptor for the carboxyl (C)-terminal portion of PTH (C-PTH receptor) in rat osteosarcoma cells, ROS 17/2.8. The Ca2+ concentration was reduced by 0.19 ± 0.03 mmol/liter over 2 h in all TPTX groups. Infusion of solvent over 2 more h had no further effect on the Ca2+ concentration (−0.01 ± 0.01 mmol/liter), whereas infusion of hPTH-(7–84) or a fragment mixture [10% hPTH-(7–84) and 45% each of hPTH-(39–8...

/pdf/synthetic-carboxyl-terminal-fragments-of-parathyroid-hormone-3d4x8a0wao.pdf

Synthetic Carboxyl-Terminal Fragments of Parathyroid Hormone (PTH) Decrease Ionized Calcium Concentration in Rats by Acting on a Receptor Different from the PTH/PTH-Related Peptide Receptor

The PTH2 receptor is a G protein-coupled receptor selectively activated by PTH. We are studying the receptors distribution to guide the investigation of its physiological function. We have now generated an antibody from a C-terminal peptide sequence of the PTH2 receptor and used this to study its cellular distribution. Labeling with the antibody identified a number of endocrine cells expressing the PTH2 receptor, including thyroid parafollicular cells, pancreatic islet D cells, and some gastrointestinal peptide synthesizing cells. There was complete overlap of PTH2 receptor labeling with somatostatin in pancreatic islets, and partial overlap with somatostatin in thyroid parafollicular cells and in the gastrointestinal tract. Furthermore, observations made previously by in situ hybridization histochemistry, including expression throughout the cardiovascular system, as well as by discrete populations of cells within the gastrointestinal tract and reproductive system were confirmed. These data suggest a broa...

Distribution of the parathyroid hormone 2 receptor in rat: immunolocalization reveals expression by several endocrine cells.

Parathyroid cancer is rare but relatively frequent in Japan compared to Western countries. Surgical parathyroidectomy is the primary choice for radical treatment of primary hyperparathyroidism (pHPT), hence it is important to distinguish malignant from benign tumor in the determination of surgical indication as well as method of operation. However, it is not easy to diagnose parathyroid cancer prior to operation. In the present study, we analyzed the background data, biochemical data and bone mineral density (BMD) of 131 patients with pHPT (111 benign and 20 malignant). BMD of the lumbar spine and mid-radius was measured by dual-energy X-ray absorptiometry. Serum levels of calcium, alkaline phosphatase (ALP), and parathyroid hormone (PTH) were significantly higher in malignant group compared to benign one. The extent of elevation of mid PTH seemed to be higher than that of intact PTH in malignant group. Age-, gender-, and race-adjusted BMD of distal one-third of radius was significantly decreased in malignant group compared to benign one, although that of lumbar spine was not significantly different between the two groups, indicating that osteopenia was marked in the region which was rich in cortical bone in malignant group. On the other hand, serum levels of calcium, ALP, and mid PTH as well as age were selected as predictors of malignancy in univariate logistic regression analysis, while serum level of intact PTH was not selected. In conclusion, radial BMD was lower in malignant group compared to benign one in pHPT. Serum levels of calcium, ALP and mid PTH were useful to predict malignancy of affected parathyroid glands in pHPT patients.

Trial to Predict Malignancy of Affected Parathyroid Glands in Primary Hyperparathyroidism

The PTH2 receptor is a recently identified G protein-coupled receptor activated by PTH. Its amino acid sequence is most similar to the PTWPTHrP receptor, but unlike the PTH/PTHrP receptor, it is activated by PTH and not by PTH-related peptide. We previously demonstrated using Northern blots that expression of PTH2 receptor messenger RNA was greatest within the brain and occurred at lower levels in pancreas, testis, and placenta. We have now obtained a complementary DNA encoding the rat PTH2 receptor and used it to study the distribution ofthe PTH2 receptor using in situ hybridization histochemistry. PTH2 receptor messenger RNA is abundantly expressed in arterial and cardiac endothelium and at lower levels in vascular smooth muscle. It is also abundant in the lung, both within bronchi and in the parenchyma, and is present within the exocrine pancreas. It is expressed by sperm in the head of the epididymis. A small number of cells associated with the vascular pole of renal glomeruli express the receptor. These data suggest that the PTH2 receptor may be responsible for PTH effects in a number of physiological systems. (Endocrinology

Distribution of Parathyroid Hormone-Z Receptor Messenger Ribonucleic Acid in Rat

We have recently demonstrated that the carboxyl-terminal (C-terminal) PTH fragments increase or decrease alkaline phosphatase activity in dexamethasone-treated ROS 17/2.8 cells, depending on the length of deletion of amino-terminal amino acids of the PTH molecule, and interact with amino-terminal (N-terminal) PTH fragment [Acta Endocrinol 128:367]. In the present study, we examined individual and combined inhibitory effects of N-terminal and a series of truncated C-terminal PTH fragments [PTH (1-34), (35-84), (53-84) and (71-84)] on the binding of intact PTH molecule [PTH (1-84)] to ROS 17/2.8 cells. The C-terminal PTH fragments, as well as the N-terminal PTH fragment, partially inhibited the binding of [35S]-labeled PTH (1-84) to the cells. The inhibitory effect of C-terminal PTH fragments was reduced along with the deletion of aminoterminal amino acids of the PTH molecule, but still retained in the shortest C-terminal PTH fragment, PTH (71-84). When added together, PTH (1-34) reinforced the inhibitory effect of each C-terminal PTH fragment. The combination of PTH (1-34) and the complementary C-terminal PTH fragment, PTH (35-84), resulted in inhibition of [35S] PTH (1-84) binding to the level obtained by addition of the same concentration of unlabeled PTH (1-84). These findings suggested that the region relatively close to the C-terminal end of the PTH molecule might be essential for the binding of C-terminal PTH fragment could be responsible for the modification of the binding affinity of the peptide to the receptor and the action of the peptide.

Binding of the carboxyl-terminal fragments of human parathyroid hormone to rat osteoblastic cells ROS 17/2.8

Chronic renal failure is associated with structural and functional abnormalities of the exocrine system of the pancreas. Certain data suggest that the excess parathyroid hormone (PTH) in these patients may participate in the genesis of these pancreatic derangements. However, direct evidence that PTH exerts a direct effect on the exocrine pancreatic system is not well documented. The present study examined the effects of the intact molecule (1–84 PTH) and of the amino-terminal fragment (1–34 PTH) of the hormone on the basal output of pure pancreatic juice (PPJ) volume and pancreatic protein secretion in the rat. 1–84 PTH but not 1–34 PTH significantly (p

Acute administration of intact parathyroid hormone but not its amino-terminal fragment stimulates volume of pancreatic secretion.

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Acute administration of intact parathyroid hormone but not its amino-terminal fragment stimulates volume of pancreatic secretion.