Bcl-2 Modulates Endoplasmic Reticulum and Mitochondrial Calcium Stores in PC12 Cells

Endoplasmic reticulum (ER) and mitochondria are intracellular organelles and their interactions are directly involved in different processes such as Ca2+ signaling in cell survival and death mechanisms. Bcl-2 is an anti-apoptotic protein intrinsically related to ER and mitochondria, modulating Ca2+ content in these organelles. We investigated the effects of Bcl-2 overexpression on ER and mitochondrial Ca2+ dynamics in PC12 cells. Bcl-2 overexpressing and control cells were loaded with Fura 2/AM and stimulated with different drugs. Results showed that in Bcl-2 cells, ACh induced a lower Ca2+ response compared to control. Ca2+ release induced by TG was decreased in Bcl-2 cells, however, it was greater in Caff induced Ca2+ rise. In addition, FCCP induced a higher Ca2+ release in Bcl-2 cells. These results suggest that Bcl-2 overexpression modulate the ER Ca2+ pools differently and the release of ER Ca2+ may increase mitochondrial Ca2+ accumulation. These alterations of intracellular Ca2+ stores are important mechanisms for the control of Ca2+ signaling.