scholarly journals Effects of Orai3-Mediated Store-Operated Calcium Entry on Parathyroid Hormone Release in Secondary Hyperparathyroidism

2021 ◽  
Author(s):  
Zhangying Lin ◽  
Shuhao Wang ◽  
Yanxun Han ◽  
Junwei Zhu ◽  
Suwen Bai ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Tumor Development ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Common Complication ◽  
Store Operated Calcium Entry ◽  
Serum Pth ◽  
Parathyroid Hormone Release

Abstract Secondary hyperparathyroidism (SHPT) is a common complication of chronic kidney disease, is characterized by elevated parathyroid hormone (PTH) secretion and Hypocalcemia. Orai3 is a highly selective calcium (Ca2+) channel that plays important roles in tumor development, cardiovascular disease, and autoimmune diseases; however, its role in SHPT is unclear. In the present study, RNA sequencing and western blot assays were used to detect the expression levels of Orai3 in parathyroid tissue from patients with SHPT and from individuals without SHPT. Ca2+ imaging was used to detect the effect of Orai3 channels on Ca2+ signaling in parathyroid gland cells. Enzyme-linked immunosorbent assays were used to detect changes in PTH release. Orai3 knockout rats were used to detect the effect of decreased Orai3 expression on serum PTH levels. We found that the expression of Orai3 in parathyroid tissue obtained from patients with SHPT was significantly higher than that in patients without SHPT. Knockdown of Orai3 in parathyroid cells by transfection with Orai3-specific small inhibitor RNA inhibited store-operated Ca2+ entry (SOCE) in parathyroid cells. Inhibition of SOCE or knockdown of Orai3 significantly inhibited PTH release in parathyroid cells. PTH levels in the blood of Orai3 knockout rat were significantly reduced. Therefore, Orai3 expression and Orai3-mediated Ca2+ signaling may be a mechanism underlying PTH release, and Orai3 may play a role in the development of SHPT.

scholarly journals Calcium-regulated parathyroid hormone release in patients with mild or advanced secondary hyperparathyroidism

1995 ◽  
Vol 48 (5) ◽  
pp. 1553-1558 ◽  
Author(s):  
William G. Goodman ◽  
Tom Belin ◽  
Barbara Gales ◽  
Harald Juppner ◽  
Gino V. Segre ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Hormone Release ◽  
Parathyroid Hormone Release

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

1984 ◽  
Vol 105 (3) ◽  
pp. 354-359 ◽  
Author(s):  
Claes Rudberg ◽  
Göran Åkerström ◽  
Henry Johansson ◽  
Sverker Ljunghall ◽  
Jan Malmaeus ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Parathyroid Tissue ◽  
Vitamin D Metabolites ◽  
Hormone Release ◽  
High Doses ◽  
Parathyroid Hormone Release ◽  
Dispersed Cells

Abstract. The effects of 125-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.

Dopamine-stimulated parathyroid hormone release in vitro: further evidence for a two-pool model of parathyroid hormone secretion

1985 ◽  
Vol 63 (9) ◽  
pp. 1139-1144 ◽  
Author(s):  
David A. Hanley ◽  
Paul G. Wellings
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Low Calcium ◽  
Pool Model ◽  
Parathyroid Hormone Release ◽  
Perifusion System ◽  
Sustained Increase

Bovine parathyroid tissue was placed in an in vitro perifusion system for the study of parathyroid hormone secretion stimulated by low calcium and dopamine. Dopamine caused a transient increase in parathyroid hormone release, while low calcium caused a sustained increase in parathyroid hormone secretion. The dopamine response was similar to that caused by isoproterenol. After parathyroid hormone release had been stimulated by dopamine there was no response to isoproterenol, suggesting they cause the release of the same cellular pool of hormone. Inhibition of protein synthesis with cycloheximide eliminated the response to low calcium, with no effect on dopamine-stimulated parathyroid hormone release. These studies suggest dopamine stimulates the release of a limited quantity storage pool of parathyroid hormone, while low calcium causes a sustained release of hormone by stimulating secretion of newly synthesized hormone. Low calcium has little or no effect on release of the storage granule pool of parathyroid hormone.

scholarly journals Parathyroid carcinoma arising from auto-transplanted parathyroid tissue after Total Parathyroidectomy in chronic kidney disease patient: a case report

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Ho-Ryun Won ◽  
Jae Yoon Kang ◽  
In Ho Lee ◽  
Jin-Man Kim ◽  
Jae Won Chang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Parathyroid Carcinoma ◽  
Parathyroid Tissue ◽  
Adjuvant Radiation ◽  
Total Parathyroidectomy ◽  
Pharmacologic Treatment ◽  
Remarkable Case

Abstract Background Secondary hyperparathyroidism is a common complication in patients with chronic kidney disease that requires vigilant treatment due to its high mortality rate. Pharmacologic therapy is recommended as an initial treatment; if there is no response, a total parathyroidectomy is performed. In some cases, surgery is accompanied by auto-transplantation of parathyroid tissue. Case presentation The patient was diagnosed with chronic kidney disease and received a kidney transplant. However, due to rejection of the transplanted kidney, medical nephrectomy was carried out and routine hemodialysis was initiated and observed. At this time, secondary hyperparathyroidism with elevated parathyroid hormone and hyperphosphatemia developed and pharmacologic treatment was applied. However, there was no response to pharmacologic treatment; therefore, total parathyroidectomy with auto-transplantation was performed. Eight years after surgery, a growing mass was observed in the transplantation site, accompanied by an elevation of parathyroid hormone. A complete resection of the mass was performed, and the patient was diagnosed with parathyroid carcinoma. Additional adjuvant radiation therapy was ordered, and the patient is being monitored. Conclusions This is a rare but remarkable case of parathyroid carcinoma arising from auto-transplanted parathyroid tissue after total parathyroidectomy in a patient with secondary hyperparathyroidism. We suggest caution should be taken when choosing to auto- transplant parathyroid tissue and that careful postoperative observation should be performed.

scholarly journals Suppressive effect of calcium on parathyroid hormone release in adynamic renal osteodystrophy and secondary hyperparathyroidism

1997 ◽  
Vol 51 (5) ◽  
pp. 1590-1595 ◽  
Author(s):  
William G. Goodman ◽  
Johannes D. Veldhuis ◽  
Thomas R. Belin ◽  
Harald Juppner ◽  
Isidro B. Salusky
Keyword(s):  
Parathyroid Hormone ◽  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Suppressive Effect ◽  
Hormone Release ◽  
Parathyroid Hormone Release
Sign in / Sign up

Export Citation Format

Share Document