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

Ichiro Yoshida, Akira Monji, Ken ichiro Tashiro, Kei ichiro Nakamura, Ryuji Inoue, Shigenobu Kanba

Research output: Contribution to journalArticle

73 Citations (Scopus)

Abstract

The mechanisms of intracellular calcium store depletion and store-related Ca2+ 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 Ca2+ by BAPTA/AM (50 μM), or La3+ (100 μM) enhanced while dantrolene (100 μM) 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 Ca2+ 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 Ca2+ concentrations ([Ca2+]i).

Original languageEnglish
Pages (from-to)696-702
Number of pages7
JournalNeurochemistry International
Volume48
Issue number8
DOIs
Publication statusPublished - Jun 2006

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

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