fura-pe3 and Nerve-Degeneration

fura-pe3 has been researched along with Nerve-Degeneration* in 1 studies

Other Studies

1 other study(ies) available for fura-pe3 and Nerve-Degeneration

Article	Year
Depletion of intracellular Ca2+ store itself may be a major factor in thapsigargin-induced ER stress and apoptosis in PC12 cells. Neurochemistry international, 2006, Volume: 48, Issue:8 The mechanisms of intracellular calcium store depletion and store-related Ca(2+) dysregulation in relation to apoptotic cell death in PC12 cells were investigated at physiological temperatures with a leak-resistant fluorescent indicator dye Fura-PE3/AM by a cooled CCD imaging analysis system. Electron microscopic observations have shown thapsigargin (TG; 100 nM)-induced apoptosis in PC12 cells. Thorough starvation of stored Ca(2+) by BAPTA/AM (50 microM), or La(3+) (100 microM) enhanced while dantrolene (100 microM) attenuated the TG-induced apoptosis by preventing a calcium release from internal stores. An immunoblotting analysis revealed an enhanced expression of GRP78, the hallmark of endoplasmic reticulum (ER) stress when cells were treated by TG along with BAPTA/AM. These results indicate that the depletion of the intracellular Ca(2+) stores itself induces the ER stress and apoptosis in PC12 cells without any involvement of the capacitative calcium entry (CCE) or a sustained elevation of intracellular Ca(2+) concentrations ([Ca(2+)](i)). Topics: Animals; Apoptosis; Calcium; Calcium Signaling; Chelating Agents; Dantrolene; Endoplasmic Reticulum; Enzyme Inhibitors; Fura-2; Heat-Shock Proteins; Homeostasis; Intracellular Fluid; Lanthanum; Molecular Chaperones; Muscle Relaxants, Central; Nerve Degeneration; Neurons; PC12 Cells; Rats; Stress, Physiological; Thapsigargin	2006

Article

Year

Depletion of intracellular Ca2+ store itself may be a major factor in thapsigargin-induced ER stress and apoptosis in PC12 cells.

Neurochemistry international, 2006, Volume: 48, Issue:8

The mechanisms of intracellular calcium store depletion and store-related Ca(2+) dysregulation in relation to apoptotic cell death in PC12 cells were investigated at physiological temperatures with a leak-resistant fluorescent indicator dye Fura-PE3/AM by a cooled CCD imaging analysis system. Electron microscopic observations have shown thapsigargin (TG; 100 nM)-induced apoptosis in PC12 cells. Thorough starvation of stored Ca(2+) by BAPTA/AM (50 microM), or La(3+) (100 microM) enhanced while dantrolene (100 microM) attenuated the TG-induced apoptosis by preventing a calcium release from internal stores. An immunoblotting analysis revealed an enhanced expression of GRP78, the hallmark of endoplasmic reticulum (ER) stress when cells were treated by TG along with BAPTA/AM. These results indicate that the depletion of the intracellular Ca(2+) stores itself induces the ER stress and apoptosis in PC12 cells without any involvement of the capacitative calcium entry (CCE) or a sustained elevation of intracellular Ca(2+) concentrations ([Ca(2+)](i)).

Topics: Animals; Apoptosis; Calcium; Calcium Signaling; Chelating Agents; Dantrolene; Endoplasmic Reticulum; Enzyme Inhibitors; Fura-2; Heat-Shock Proteins; Homeostasis; Intracellular Fluid; Lanthanum; Molecular Chaperones; Muscle Relaxants, Central; Nerve Degeneration; Neurons; PC12 Cells; Rats; Stress, Physiological; Thapsigargin

2006