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

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 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

Normalizing effect of Ca2+ ionophore on cytoplasmic Ca2+ and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism

1986 ◽  
Vol 45 (2-3) ◽  
pp. 191-196 ◽  
Author(s):  
Rolf Larsson ◽  
Chris Wallfelt ◽  
Göran Åkerström ◽  
Sverker Ljunghall ◽  
Jonas Rastad ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Release ◽  
Parathyroid Hormone Release
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