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The effects of calcium channel blockers on nuclear factor kappa B activation in the mesangium cells

M Hayashi1, Y Yamaji, Y Nakazato

  • 1Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.

Hypertension Research : Official Journal of the Japanese Society of Hypertension
|October 4, 2000
PubMed

Insights

Calcium channel blockers (CCBs) inhibit nuclear factor kappa B (NFkappaB) activation, a key signaling pathway. This effect is independent of L-type calcium channels and varies among different CCBs.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Pharmacology

Background:

  • Calcium channel blockers (CCBs) are known to inhibit cell growth and transcriptional changes.
  • Nuclear factor kappa B (NFkappaB) is a critical transcription factor in intracellular signaling pathways regulated by cytokines and hormones.

Purpose of the Study:

  • To investigate the effects of CCBs on the activity of NFkappaB.
  • To determine if CCBs modulate NFkappaB signaling independently of L-type calcium channels.

Main Methods:

  • NFkappaB activity was measured using a luciferase reporter assay in cultured human mesangial cells.
  • Cells were stimulated with calcium ionophore (A23187) or phorbol ester (PMA).
  • The effects of L-type calcium channel agonist (Bay K 8644) and various CCBs (nifedipine, verapamil, efonidipine) were assessed.

Main Results:

  • Increased intracellular calcium stimulated PMA-induced NFkappaB activation.
  • L-type calcium channel agonist did not affect basal or stimulated NFkappaB activity.
  • CCBs (nifedipine, verapamil, efonidipine) inhibited NFkappaB activation by PMA and A23187 in a dose-dependent manner, with efonidipine showing effects at lower concentrations.

Conclusions:

  • CCBs exert an inhibitory effect on NFkappaB activation through a pathway independent of L-type calcium channels.
  • The potency of this inhibitory effect varies among different CCBs.

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