scholarly journals Regulation of E-cadherin and β-catenin by Ca2+ in colon carcinoma is dependent on calcium-sensing receptor expression and function

2007 ◽  
Vol 121 (7) ◽  
pp. 1455-1462 ◽  
Author(s):  
Narasimharao Bhagavathula ◽  
Andrew W. Hanosh ◽  
Kamalakar C. Nerusu ◽  
Henry Appelman ◽  
Subhas Chakrabarty ◽  
...  
Keyword(s):  
Colon Carcinoma ◽  
Receptor Expression ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
And Function ◽  
E Cadherin

scholarly journals Reversal of Secondary Hyperparathyroidism by Phosphate Restriction Restores Parathyroid Calcium-Sensing Receptor Expression and Function

2002 ◽  
Vol 17 (12) ◽  
pp. 2206-2213 ◽  
Author(s):  
Cynthia S. Ritter ◽  
Daniel R. Martin ◽  
Yan Lu ◽  
Eduardo Slatopolsky ◽  
Alex J. Brown
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Receptor Expression ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
And Function

Expression and function of the calcium sensing receptor (CaR) in gastrinomas

2000 ◽  
Vol 118 (4) ◽  
pp. A297
Author(s):  
Stephan U. Goebel ◽  
Paolo L. Peghini ◽  
Paul Goldsmith ◽  
Allen M. Spiegel ◽  
Fathia Gibril ◽  
...  
Keyword(s):  
Calcium Sensing Receptor ◽  
Calcium Sensing ◽  
And Function

scholarly journals The calcium-sensing receptor and vitamin D receptor expression in tertiary hyperparathyroidism

2006 ◽  
Author(s):  
Tomasz Grzela ◽  
Witold Chudzinski ◽  
Zofia Lasiecka ◽  
Justyna Niderla ◽  
Grzegorz Wilczynski ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Receptor ◽  
Receptor Expression ◽  
Calcium Sensing Receptor ◽  
Tertiary Hyperparathyroidism ◽  
Calcium Sensing

scholarly journals Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism

2005 ◽  
Vol 153 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Takehisa Kawata ◽  
Yasuo Imanishi ◽  
Keisuke Kobayashi ◽  
Takao Kenko ◽  
Michihito Wada ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Murine Model ◽  
Hormone Secretion ◽  
Suppressive Effect ◽  
Receptor Expression ◽  
Parathyroid Glands ◽  
Calcium Sensing Receptor ◽  
Calcium Sensing

Cinacalcet HCl, an allosteric modulator of the calcium-sensing receptor (CaR), has recently been approved for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, due to its suppressive effect on parathyroid hormone (PTH) secretion. Although cinacalcet’s effects in patients with primary and secondary hyperparathyroidism have been reported, the crucial relationship between the effect of calcimimetics and CaR expression on the parathyroid glands requires better understanding. To investigate its suppressive effect on PTH secretion in primary hyperparathyroidism, in which hypercalcemia may already have stimulated considerable CaR activity, we investigated the effect of cinacalcet HCl on PTH-cyclin D1 transgenic mice (PC2 mice), a model of primary hyperparathyroidism with hypo-expression of CaR on their parathyroid glands. A single administration of 30 mg/kg body weight (BW) of cinacalcet HCl significantly suppressed serum calcium (Ca) levels 2 h after administration in 65- to 85-week-old PC2 mice with chronic biochemical hyperparathyroidism. The percentage reduction in serum PTH was significantly correlated with CaR hypo-expression in the parathyroid glands. In older PC2 mice (93–99 weeks old) with advanced hyperparathyroidism, serum Ca and PTH levels were not suppressed by 30 mg cinacalcet HCl/kg. However, serum Ca and PTH levels were significantly suppressed by 100 mg/kg of cinacalcet HCl, suggesting that higher doses of this compound could overcome severe hyperparathyroidism. To conclude, cinacalcet HCl demonstrated potency in a murine model of primary hyperparathyroidism in spite of any presumed endogenous CaR activation by hypercalcemia and hypo-expression of CaR in the parathyroid glands.

Calcitriol Prevents In Vitro Vascular Smooth Muscle Cell Mineralization by Regulating Calcium-Sensing Receptor Expression

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 1965-1974 ◽  
Author(s):  
Aurélien Mary ◽  
Lucie Hénaut ◽  
Cédric Boudot ◽  
Isabelle Six ◽  
Michel Brazier ◽  
...  
Keyword(s):  
Vitamin D ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Small Interfering Rna ◽  
Receptor Expression ◽  
Calcium Sensing Receptor ◽  
Down Regulation ◽  
Calcium Sensing ◽  
Cardiovascular Morbidity And Mortality ◽  
Interfering Rna

Abstract Vascular calcification (VC) is a degenerative disease that contributes to cardiovascular morbidity and mortality. A negative relationship has been demonstrated between VC and calcium sensing receptor (CaSR) expression in the vasculature. Of interest, vitamin D response elements, which allow responsiveness to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], are present in the promoters of the CaSR gene. We hypothesized that 1,25(OH)2D3, by modulating CaSR expression in vascular smooth muscle cells (VSMCs), might protect against VC. Human VSMCs were exposed to increasing concentrations of 1,25(OH)2D3 (0.01–10 nmol/L) in noncalcifying (1.8 mmol/L) or procalcifying Ca2+0 condition (5.0 mmol/L). Using quantitative RT-PCR and Western blotting we observed a significant increase in both CaSR mRNA and protein levels after exposure to 1.0 nmol/L 1,25(OH)2D3. This effect was associated with a maximal increase in CaSR expression at the cell surface after 48 hours of 1,25(OH)2D3 treatment, as assessed by flow cytometry. Down-regulation of the vitamin D receptor by small interfering RNA abolished these effects. In the procalcifying condition, 1.0 nmol/L 1,25(OH)2D3 blocked the Ca2+0-induced decrease in total and surface CaSR expression and protected against mineralization. Down-regulation of CaSR expression by CaSR small interfering RNA abolished this protective effect. 1,25(OH)2D3 concentrations of 0.5 and 5.0 nmol/L were also effective, but other (0.01, 0.1, and 10 nmol/L) concentrations did not modify CaSR expression and human VSMC mineralization. In conclusion, these findings suggest that nanomolar concentrations of 1,25(OH)2D3 induce a CaSR-dependent protection against VC. Both lower and higher concentrations are either ineffective or may even promote VC. Whether this also holds true in the clinical setting requires further study.

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