Mitochondria sense with different kinetics the calcium entering into HeLa cells through calcium channels CALHM1 and mutated P86L-CALHM1

作者：Moreno Ortega Ana J; Ruiz Nuno Ana; Garcia Antonio G; Cano Abad Maria F^*

来源：Biochemical and Biophysical Research Communications, 2010, 391(1): 722-726.

DOI：10.1016/j.bbrc.2009.11.127

• Calcium
• Mitochondria
• CALHM1
• Alzheimer
• Aequorin

The novel Ca(2+) channel CALHM1 (Calcium Homeostasis Modulator I generates cytosolic Ca(2+) transients ([Ca(2+)](c)) that regulate the production of amyloid beta (A beta). Its mutated channel P86L-CALHM1 I 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 Ca(2+) entering into Hela cells and the Ca(2+) released from the endoplasmic reticulum (ER), in control and in cells transfected with CALIN I and P86L-CALHM1 We have shown that mitochondria sense Ca(2+) entry in the three cell types; however. the [Ca(2+)](c) and mitochondrial Ca(2+) transients [Ca(2+)](m) had substantially slower kinetics in cells expressing P86L-CALHM1 Mitochondria also sensed the ER Ca(2+) released by histamine. but ill CALHM1 and P86L-CALHM1 cells the kinetics was faster than that of control cells. Data are com

• 出版日期2010-1-1