Premium
Evidence for a pertussis toxin sensitive calcium entry pathway in thyroid FRTL‐5 cells
Author(s) -
Törnquist Kid,
Ekokoski Elina
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041640118
Subject(s) - pertussis toxin , purinergic receptor , calcium , protein kinase c , chemistry , extracellular , t type calcium channel , calcium atpase , phospholipase c , stimulation , second messenger system , endocrinology , g protein , voltage dependent calcium channel , medicine , microbiology and biotechnology , biology , receptor , biochemistry , signal transduction , atpase , enzyme , organic chemistry
Receptor‐mediated calcium entry was investigated in Fura 2 loaded FRTL‐5 cells. The purinergic agonist ATP activated the release of sequestered calcium and the entry of extracellular calcium. Downregulation of protein kinase C (PKC) substantially enhanced the ATP‐evoked calcium entry. Pretreatment of the cells with pertussis toxin (Ptx) decreased the ATP‐evoked calcium entry by 56% and the release of sequestered calcium by 34%. In PKC‐downregulated cells, the effect of Ptx treatment on the ATP‐evoked increase in [Ca 2+ ] i was 73% and 44%, respectively. Phorbol myristic acetate (PMA) decreased the ATP‐evoked calcium entry to the same extent as Ptx. In Ptx‐treated cells, the ATP‐evoked influx of 45 Ca 2+ was attenuated. Stimulation of the cells with P 2p ‐purinergic agonist GTP evoked no entry of calcium, although GTP released the same amount of sequestered calcium as did ATP. PKC downregulation or pretreatment with Ptx had no effects on the GTP‐evoked responses, whereas PMA decreased the GTP‐evoked release of calcium. We conclude that the ATP‐activated rapid calcium entry pathway is a second messenger‐operated calcium channel. © 1995 Wiley‐Liss, Inc.