[3H]-thymidine labelling of DNA triggers apoptosis potentiated by E1A-adenoviral protein

Serge N. Orlov, D. V. Pchejetski, S. D. Sarkissian, V. Adarichev, S. Taurin, A. V. Pshezhetsky, J. Tremblay, G. V. Maximov, D. DeBlois, M. R. Bennett, P. Hamet

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


[3H]-thymidine is commonly used to analyze the accumulation of [3H]-labeled chromatin fragments in cells undergoing apoptosis. This study shows that [3H]-thymidine incorporation within DNA is sufficient per se to inhibit growth and to induce apoptosis in canine kidney epithelial cells and porcine aorta endothelial cells. Despite highlevel [3H]-thymidine-DNA labeling, rat vascular smooth muscle cells (VSMC) showed only modest inhibition of growth and induction of apoptosis compared to other cell types. Similarly to serum deprivation, apoptosis triggered by [3H]-thymidine labeling was sharply potentiated by VSMC transfection with a functional analogue of c-myc, E1A-adenoviral protein (VSMC-E1A), and was suppressed by stimulation of cAMP signaling with forskolin as well as by and Na/K pump inhibition with ouabain. Both apoptosis induction and growth suppression seen in [3H]-thymidine-treated VSMC-E1A were reduced by the pancaspase inhibitor z-VAD.fmk. Thus, our results show that the differential efficiency of the apoptotic machinery determines cell type-specific attenuation of growth in cells with [3H]-thymidine-labeled DNA. They also demonstrate that [3H]-thymidine-treated and serum-deprived VSMC employ common intermediates of the apoptotic machinery, including steps that are potentiated by E1A-adenoviral protein and inhibited by activation of cAMP signaling as well as by inversion of the intracellular [Na+]i/[K+]i ratio.

Original languageEnglish
Pages (from-to)199-208
Number of pages10
Issue number2
Publication statusPublished - Mar 2003


  • Apoptosis
  • Cell growth
  • E1A adenoviral protein
  • [H]-thymidine

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Cancer Research

Fingerprint Dive into the research topics of '[<sup>3</sup>H]-thymidine labelling of DNA triggers apoptosis potentiated by E1A-adenoviral protein'. Together they form a unique fingerprint.

Cite this