Calcium oscillation induced by bradykinin in polyoma middle T antigen-transformed NIH3T3 fibroblasts: evidence for

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Y Okano1, T Fu, Y Nozawa

  • 1Department of Biochemistry, Gifu University School of Medicine, Japan.

Biochemical and Biophysical Research Communications
|April 30, 1991
PubMed

Insights

Bradykinin induces calcium oscillations in transformed cells, dependent on extracellular calcium entry and protein kinase C. Spontaneous oscillations also occur, unaffected by protein kinase C modulation.

Area of Science:

  • Cell Biology
  • Calcium Signaling

Background:

  • Bradykinin (BK) is a peptide that elicits various cellular responses.
  • Intracellular calcium ([Ca2+]i) plays a critical role in cell signaling pathways.
  • Transformed cell lines can exhibit altered signaling compared to their parental counterparts.

Purpose of the Study:

  • To investigate the role of bradykinin in inducing intracellular calcium oscillations in polyoma middle T-transformed MT3 cells.
  • To elucidate the mechanisms underlying BK-induced calcium oscillations, including calcium source and involvement of protein kinase C (PKC).
  • To characterize spontaneous calcium oscillations in MT3 cells.

Main Methods:

  • Utilized calcium imaging techniques to monitor intracellular free calcium ([Ca2+]i) levels.
  • Applied bradykinin as a stimulus in polyoma middle T-transformed MT3 cells and parental NIH3T3 cells.
  • Employed calcium channel blockers (SK&F 96365, CdCl2), phorbol myristate acetate (PMA), and a PKC inhibitor (H-7) to investigate signaling pathways.

Main Results:

  • Bradykinin triggered long-lasting intracellular calcium oscillations in MT3 cells, but not in NIH3T3 cells.
  • BK-induced oscillations were dependent on extracellular calcium and inhibited by calcium channel blockers, suggesting receptor-operated calcium entry.
  • Phorbol myristate acetate (PMA) abolished BK-induced oscillations, an effect reversed by a protein kinase C (PKC) inhibitor (H-7), indicating PKC involvement.
  • Spontaneous calcium oscillations were observed in some MT3 cells, were extracellular calcium-dependent, but were not affected by PMA or H-7.

Conclusions:

  • Bradykinin-induced calcium oscillations in MT3 cells are mediated by extracellular calcium influx through a receptor-operated channel and involve protein kinase C.
  • Spontaneous calcium oscillations in MT3 cells represent a distinct pathway, independent of PKC and agonist stimulation.
  • These findings highlight differential calcium signaling mechanisms in transformed cells.

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