Synergistic suppression of apoptosis in salivary acinar cells by IGF1 and EGF

K. H. Limesand, K. A. Barzen, D. O. Quissell, Steve M. Anderson

Research output: Contribution to journalReview articlepeer-review

27 Scopus citations


Tissue homeostasis requires balancing cell proliferation and programmed cell death. IGF1 significantly suppressed etoposide-induced apoptosis, measured by caspase 3 activation and quantitation of cellular subG1 DNA content, in rat parotid salivary acinar cells (C5). Transduction of C5 cells with an adenovirus expressing a constitutively activated mutant of Akt-suppressed etoposide-induced apoptosis, whereas a kinase-inactive mutant of Akt suppressed the protective effect of IGF1. IGF1 also suppressed apoptosis induced by taxol and brefeldin A. EGF was unable to suppress apoptosis induced by etoposide, but was able to synergize with IGF1 to further suppress caspase 3 activation and DNA cleavage after etoposide treatment. The catalytic activity of Akt was significantly higher following stimulation with both growth factors compared to stimulation with IGF1 or EGF alone. These results suggest that a threshold of activated Akt is required for suppression of apoptosis and the cooperative action of growth factors in regulating salivary gland homeostasis.

Original languageEnglish (US)
Pages (from-to)345-355
Number of pages11
JournalCell Death and Differentiation
Issue number3
StatePublished - Mar 1 2003


  • Akt
  • Apoptosis
  • EGF
  • IGF1
  • Protein kinase B
  • Salivary gland

ASJC Scopus subject areas

  • Cell Biology


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