Akt depletion is an important determinant of L929 cell death following heat stress

Sehamuddin Galadari, Faisal Thayyullathil, Abdulkader Hago, Mahendra Patel, Shahanas Chathoth

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Exposure of mammalian cells to heat stress causes impairment of numerous physiological functions and activates a number of signaling pathways. Some of these pathways, such as induction of heat-shock proteins and activation of Akt, enhance the ability of cells to survive heat stress. On the other hand, heat stress can trigger cell-death signaling via activation of the stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/Jnk). Recently, it has been shown that kinases activated by heat stress can regulate synthesis and functioning of the molecular chaperones, and these chaperones modulate the activity of the cell death and survival pathways. We have found that Akt plays a central role in determining the fate of L929 fibroblast cells exposed to heat stress. In our experiments heat stress causes Akt depletion and L929 cells to undergo cell death. Heat-shock protein 70 (Hsp70) is known to prevent stress-induced cell death by interfering with the SAPK/Jnk signaling pathway. In our study, there is a very high level of induction of Hsp70, yet this is not sufficient to rescue Akt depletion and L929 from cell death. The Akt depletion is specific, since actin protein level does not change during the heat stress. Moreover, our studies show that L929 cells can recover from a short-term heat shock, whereby, Akt level is returned to normal following recovery from heat shock. Therefore, it appears that the fate of the prolonged heat-stressed fibroblast cells is determined by Akt level, and that return of Akt protein level to normal prevents cell death.

Original languageEnglish (US)
Title of host publicationRecent Advances in Clinical Oncology
PublisherBlackwell Publishing Inc.
Pages385-392
Number of pages8
ISBN (Print)9781573317009
DOIs
StatePublished - Sep 2008

Publication series

NameAnnals of the New York Academy of Sciences
Volume1138
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • AKT depletion
  • Heat-stress response
  • L929 cell death

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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