Calcium-sensing receptor mediates Ca2+ homeostasis by modulating expression of PTH and stanniocalcin
- Authors
- Lin, C.H., Su, C.H., and Hwang, P.P.
- ID
- ZDB-PUB-131122-4
- Date
- 2014
- Source
- Endocrinology 155(1): 56-67 (Journal)
- Registered Authors
- Hwang, Pung Pung
- Keywords
- none
- MeSH Terms
-
- Animals
- Calcitonin/metabolism
- Calcium/metabolism*
- Gene Expression Regulation*
- Glycoproteins/metabolism*
- Homeostasis
- Hypocalcemia/metabolism
- In Situ Hybridization
- Oligonucleotides, Antisense/chemistry
- Parathyroid Glands/metabolism
- Parathyroid Hormone/metabolism*
- RNA, Messenger/metabolism
- Receptors, Calcium-Sensing/metabolism*
- Temperature
- Transgenes
- Zebrafish
- PubMed
- 24169558 Full text @ Endocrinology
Regulation of the synthesis and/or secretion of hypocalcemic and hypercalcemic hormones by calcium-sensing receptor (CaSR) is believed to be a major pathway for maintaining Ca2+ homeostasis in vertebrates, based primarily on findings in mammals. However, understanding the evolution of this physiological process requires that it be described in non-mammalian species. Here, we describe the use of zebrafish as a model to investigate whether CaSR contributes to body fluid Ca2+ homeostasis by regulating synthesis of hypercalcemic (PTH1 and PTH2) and hypocalcemic hormones (stanniocalcin (STC-1)). We report that PTH1, but not PTH2, increases Ca2+ uptake through stimulating the expression of the gene encoding epithelial Ca2+ channel (ecac). Furthermore, we demonstrate that CaSR, as a Ca2+ sensor, may differently affect stc-1 and pth1 expressions, thereby suppressing ecac expression and Ca2+ uptake. Finally, we show that CaSR knockdown has time-dependent effects on STC-1 and PTH1 expression, and these two hormones have mutual effects on the expressions, thus forming a possible counterbalance. These findings enhance our understanding of CaSR-PTH-STC control of Ca2+ homeostasis in vertebrates.