Distinct Signaling Pathways for Autophagy-Driven Cell Death and Survival in Adult Hippocampal Neural Stem Cells

Seol Hwa Jeong, Hyun Kyu An, Shinwon Ha, Seong Woon Yu

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Autophagy is a cellular catabolic process that degrades and recycles cellular materials. Autophagy is considered to be beneficial to the cell and organism by preventing the accumulation of toxic protein aggregates, removing damaged organelles, and providing bioenergetic substrates that are necessary for survival. However, autophagy can also cause cell death depending on cellular contexts. Yet, little is known about the signaling pathways that differentially regulate the opposite outcomes of autophagy. We have previously reported that insulin withdrawal (IW) or corticosterone (CORT) induces autophagic cell death (ACD) in adult hippocampal neural stem (HCN) cells. On the other hand, metabolic stresses caused by 2-deoxy-D-glucose (2DG) and glucose-low (GL) induce autophagy without death in HCN cells. Rather, we found that 2DG-induced autophagy was cytoprotective. By comparing IW and CORT conditions with 2DG treatment, we revealed that ERK and JNK are involved with 2DG-induced protective autophagy, whereas GSK-3β regulates death-inducing autophagy. These data suggest that cell death and survival-promoting autophagy undergo differential regulation with distinct signaling pathways in HCN cells.

Original languageEnglish
Article number8289
JournalInternational Journal of Molecular Sciences
Volume24
Issue number9
DOIs
StatePublished - May 2023

Bibliographical note

Publisher Copyright:
© 2023 by the authors.

Keywords

  • ERK
  • GSK-3β
  • JNK
  • adult hippocampal neural stem cells
  • autophagic cell death
  • autophagy

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