Moreno-Ortega 2009 Biochem Biophys Res Commun

Moreno-Ortega AJ1, Ruiz-Nuño A, García AG, Cano-Abad MF (2009) Mitochondria sense with different kinetics the calcium entering into HeLa cells through calcium channels CALHM1 and mutated P86L-CALHM1. Biochem Biophys Res Commun 391:722-6.

» PMID: 19944073

Moreno-Ortega AJ1, Ruiz-Nuno A, Garcia AG, Cano-Abad MF (2009) Biochem Biophys Res Commun

Abstract: The novel Ca²⁺ channel CALHM1 (Calcium Homeostasis Modulator 1) generates cytosolic Ca²⁺ transients ([Ca(2+)](c)) that regulate the production of amyloid beta (Abeta). Its mutated channel P86L-CALHM1 has been associated to Alzheimer's disease (AD). Using cytosolic- and mitochondrial-targeted aequorins, we have investigated here whether mitochondria sense with similar or different kinetics the Ca²⁺ entering into Hela cells and the Ca²⁺ released from the endoplasmic reticulum (ER), in control and in cells transfected with CALHM1 and P86L-CALHM1. We have shown that mitochondria sense Ca²⁺ entry in the three cell types; however, the [Ca²⁺](c) and mitochondrial Ca²⁺ transients [Ca²⁺](m) had substantially slower kinetics in cells expressing P86L-CALHM1. Mitochondria also sensed the ER Ca²⁺ released by histamine, but in CALHM1 and P86L-CALHM1 cells the kinetics was faster than that of control cells. Data are compatible with the idea that mutated CALHM1 may cause mitochondrial Ca²⁺ overload, suggesting how these cells may become more vulnerable to apoptotic stimuli.

Labels: Pathology: Alzheimer's

Tissue;cell: HeLa