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Related Experiment Videos

Regulatory volume decrease in the presence of HCO3- by single osteosarcoma cells UMR-106-01.

R A Star1, B X Zhang, P A Loessberg

  • 1Department of Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9040.

The Journal of Biological Chemistry
|September 5, 1992
PubMed
Summary
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This study reveals that bicarbonate (HCO3-) is crucial for osteosarcoma cell volume regulation, mediating both regulatory volume decrease (RVD) and regulatory volume increase (RVI) through ion transport mechanisms. The findings highlight a novel role for the sodium-bicarbonate cotransporter in cell volume control.

Area of Science:

  • Cell Biology
  • Physiology
  • Biochemistry

Background:

  • Cell volume regulation is essential for cellular homeostasis.
  • Bicarbonate (HCO3-) plays a role in intracellular pH (pHi) regulation and cell volume control.
  • Osteosarcoma cells (UMR-106-01) are a model for studying these processes.

Purpose of the Study:

  • To investigate the role of HCO3- in regulatory volume decrease (RVD) and regulatory volume increase (RVI) in UMR-106-01 cells.
  • To elucidate the specific ion transport mechanisms involved in these volume regulatory responses.
  • To demonstrate the utility of simultaneous pHi and cell volume recording in attached single cells.

Main Methods:

  • Simultaneous recording of cell volume and pHi in single UMR-106-01 osteosarcoma cells.

Related Experiment Videos

  • Exposure to hypotonic swelling to induce RVD and RVI.
  • Manipulation of extracellular ion concentrations (Na+, Cl-, HCO3-).
  • Pharmacological inhibition of ion transport pathways (e.g., K+ channels, Na+/H+ exchange, Cl-/HCO3- exchange).

    • Main Results:

    • Hypotonic swelling induced a rapid decrease in pHi and subsequent RVD, followed by a pHi increase and recovery (RVI).
    • HCO3- was essential for both RVD and RVI, even in the absence of Na+ or Cl-.
    • RVD was mediated by conductive K+ and HCO3- efflux.
    • Hypotonic RVI was dependent on Na+ influx, independent of Cl-, and inhibited by DIDS, suggesting a Na+(HCO3-)3 cotransporter.
    • Depolarization or K+ channel inhibition abolished pHi changes and RVD.

    Conclusions:

    • Bicarbonate is a key regulator of cell volume in UMR-106-01 cells, influencing both RVD and RVI.
    • RVD is primarily driven by K+ and HCO3- conductive efflux.
    • Hypotonic RVI involves a Na+(HCO3-)3 cotransporter, a novel finding in cell volume regulation.
    • The technique for simultaneous pHi and cell volume measurement is powerful for studying cell volume regulatory mechanisms.