Membrane transport properties differ following return of serum-deprived versus Ca++-deprived human fibroblasts to a proliferative state

J. T. Tupper, W. T. Ryals, P. V. Bodine

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Abstract

Human lung fibroblasts (W138) can be brought to a quiescent state by removal of serum from the medium or by lowering of the extracellular Ca++. Upon return of Ca++ or serum, the cells enter the G1 phase and progress to S within 15-18 hours. Since multiple G1 phase blocks have been demonstrated, the authors wished to determine whether the Ca++ and serum block were equivalent since previous data suggested that these two medium components may act at a common point in the initiation of proliferation. The authors have evaluated the membrane transport of 86Rb, 3-O-methylglucose, AIB, and cycloleucine following stimulation of quiescent cells by Ca++ or serum. Serum stimulation results in large increases in the influx of all the substances tested. These increases are prevented if Ca++ is absent upon serum stimulation or they are rapidly diminished following Ca++ removal. In contrast, Ca++ stimulation of Ca++-deprived cells causes little or no enhancement of any of the transport systems, yet the cells progress to S phase in a manner similar to serum-stimulated cells. These results indicate that the Ca++ and serum G0 or G1 block are not equivalent and that the serum-induced change in transport of these components does not appear necessary for successful G1 phase progression. Furthermore, the data suggest that the sequence in which Ca++ or serum are presented to the cells alters the ability of Ca++ to modulate the transport systems. Quiescent cells which are exposed to Ca++ prior to serum possess a Ca++ modulation of several transport systems. Cells which are exposed to Ca++ subsequent to serum do not appear to possess this Ca++ regulation.

Original languageEnglish (US)
Pages (from-to)29-34
Number of pages6
JournalJournal of Cellular Physiology
Volume110
Issue number1
StatePublished - 1982

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ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

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