Differential Effects of Protein Kinase C Activation on Calcium Storage and Capacitative Calcium Entry in NIH 3T3 Cells
Year: 1996
Type: article
Abstract: In NIH 3T3 cells, treatment with phorbol 12-myristate 13-acetate (PMA) reduced the release of Ca2+ by thapsigargin, but did not activate Ca2+ entry; Ca2+ influx was triggered after the residual pool was emptied by thapsigargin, and this Ca2+ influx was similar to that induced by thapsigargin in control cells. The effect of PMA was due to decreased Ca2+ storage because 1) Ca2+ release by ionomycin was similarly affected by PMA, and in both control and PMA-treated cells, ionomycin did not release Ca2+ following thapsigargin treatment; 2) PMA reduced 45Ca2+ accumulation; and 3) studies with Ca2+ indicator compartmentalized into the endoplasmic reticulum indicated that stored Ca2+ was reduced by PMA. Although PMA did not itself activate Ca2+ entry, PMA potentiated Ca2+ entry with low concentrations of cyclopiazonic acid. With a somewhat higher concentration of cyclopiazonic acid, PMA had no effect on calcium entry. Thus, protein kinase C has two apparent actions on calcium signaling in NIH 3T3 cells: 1) reduced intracellular Ca2+ storage capacity and 2) augmented calcium entry with submaximal intracellular Ca2+ pool depletion. These actions indicate a complex and potentially important role for the protein kinase C system in calcium homeostasis in this cell type.
Source: Journal of Biological Chemistry
Authors: Carla M. Pedrosa Ribeiro, James W. Putney
Language: English
Topic: Ion Channels and Receptors
Subfield: Sensory Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Estimated APC paid: $3,430
OpenAlex ID: W2090160768