The effect of rottlerin in calcium regulation in HMC-1560 cells is mediated by a PKC-δ independent effect
✍ Scribed by Eva Alonso; Amparo Alfonso; Kristin Löber; Luis M. Botana
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 246 KB
- Volume
- 105
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
The human mast cell line (HMC‐1^560^) is a good model for Ca^2+^ signaling studies, because intracellular alkalinization is the mainly histamine release stimulus without changes in the intracellular Ca^2+^ levels. This fact allows us to study Ca^2+^ changes without degranulation, since this process can affected cellular viability. Ionomycin and thapsigargin have been fully used for induced Ca^2+^ influx across SOC channels. When HMC‐1^560^ cells are incubated with rottlerin, 5 µM, for 5 min a strong inhibition of ionomycin‐induced Ca^2+^ influx is observed. However, when thapsigargin stimulates Ca^2+^ influx, rottlerin did not show any effect on Ca^2+^ levels. This fact point two possibilities, ionomycin and thapsigargin might activate different SOC channels or that these drugs might activate the same channel but in a different way in HMC‐1^560^ cells. The rottlerin inhibition of ionomycin‐induced Ca^2+^ influx is PKC‐δ independent and this effect is not related with the store depletion, since rottlerin has the same effect when it is added before or after the stores are empty. FCCP, a know uncoupler of oxidative phosphorylation in mitochondria, induces the same inhibition in ionomycin Ca^2+^ influx than rottlerin which point to the mitochondria as a cellular target to rottlerin. J. Cell. Biochem. 105: 255–261, 2008. © 2008 Wiley‐Liss, Inc.