Inhibition of BALB/c-3T3 cells in late G1: commitment to DNA synthesis controlled by somatomedin C

J Cell Physiol. 1981 Apr;107(1):31-9. doi: 10.1002/jcp.1041070105.

Abstract

Methylglyoxal bis-(guanylhydrazone) (mGBG) blocked the stimulation of DNA synthesis in quiescent, density-inhibited BALB/c-3T3 cells treated with platelet-derived growth factor (PDGF) and platelet-poor plasma (PPP). Competence formation produced by a transient exposure to PDGF was not effected by mGBG. In contrast, mGBG effectively inhibited the PPP-stimulated progression of competent cells through the G1 phase of the cell cycle, although maximal inhibition was observed when mGBG was present during both the exposure to PDGF- and PPP-supplemented media. When quiescent cells were treated with PDGF and PPP-supplemented media in the presence of mGBG for 12--18 hours and the mGBG was then removed, cells entered the S phase after a 4 hour lag. The rate of entry into the S phase, but not the time necessary for the cells to progress from the mGBG block into the S phase, was dependent on the concentration of PPP present after removal of the mGBG. Either somatomedin C or insulin, but not epidermal growth factor, fibroblast growth factor, or PDGF were able to substitute for PPP in allowing cells to enter the S phase after the cells were released from the mGBG block. A marked inhibition of (3H)-leucine incorporation in serum-stimulated cultures was produced at mGBG concentrations which caused no decrease in the amount of (3H)-uridine incorporated during a short (15 minute) pulse. The ability of hormones to allow cells to progress to the late G1 phase and become committed to DNA synthesis after a mGBG inhibition was not related to their ability to restore the normal rate of protein synthesis as determined by (3H)-leucine incorporation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Cell Division
  • Clone Cells / cytology
  • DNA / biosynthesis
  • DNA Replication / drug effects*
  • Growth Substances / pharmacology
  • Humans
  • Insulin-Like Growth Factor I
  • Interphase / drug effects*
  • Leucine / metabolism
  • Mitoguazone / pharmacology
  • Peptides / pharmacology
  • Platelet-Derived Growth Factor
  • Somatomedins / pharmacology*

Substances

  • Growth Substances
  • Peptides
  • Platelet-Derived Growth Factor
  • Somatomedins
  • Insulin-Like Growth Factor I
  • DNA
  • Leucine
  • Mitoguazone