Role of the cytoskeleton in extracellular calcium-regulated PTH release |
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Authors: | Quinn Stephen J Kifor Olga Kifor Imre Butters Robert R Brown Edward M |
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Institution: | Division of Endocrinology, Diabetes and Hypertension and the Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. squinn@rics.bwh.harvard.edu |
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Abstract: | The calcium-sensing receptor (CaR) mediates the effects of extracellular calcium (Ca(2+)](o)) on PTH release, such that increasing levels of Ca(2+)](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 Ca(2+)](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. |
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Keywords: | Calcium-sensing receptor PTH Calcium Cytoskeleton Parathyroid cells |
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