Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 354, Issue 1, Pages 8-13Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2006.12.160
Keywords
calcium-sensing receptor; PTH; calcium; cytoskeleton; parathyroid cells
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Funding
- NIDDK NIH HHS [DK067155, DK0952005] Funding Source: Medline
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The calcium-sensing receptor (CaR) mediates the effects of extracellular calcium ([Ca2+](o)) on PTH release, such that increasing levels of [Ca2+](o) inhibit PTH secretion through poorly defined mechanisms. In the present studies, immunocytochemical analysis demonstrated that F-actin, PTH, CaR, and caveolin-1 are colocalized at the apical secretory pole of PT cells, and subcellular fractionation of PT cells showed these proteins to be present within the secretory granule fraction. High [Ca2+](o) caused F-actin, PTH, and caveolin-1 to move to the apical pole of the cells. Depolymerization of F-actin by cytochalasin reduced the actin network and induced redistribution of actin/caveolin-1 to a dispersed pattern within the cell. The F-actin-severing compounds, latrunculin and cytochalasin, significantly increased PTH secretion, while the actin polymerizing agent, jasplakinolide, substantially inhibited PTH secretion. We have demonstrated that in polarized PT cells, the F-actin cytoskeleton is involved in the regulation of PTH secretion and is critical for inhibition of PTH secretion by high calcium. (c) 2006 Elsevier Inc. All rights reserved..
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