Key result
Depletion of intracellular Ca2+ stores with thapsigargin increased nuclear phospho-CREB levels and c-fos transcription, effects that were abolished by inhibiting store-operated Ca2+ entry.
Population
Cultured vascular smooth muscle cells and intact arteries
Design
Preclinical
Authors
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May implicate store-operated Ca2+ entry in vascular gene regulation; leaves open its role in human arterial remodeling or hypertension.
Store-operated Ca2+ entry activates the CREB transcription factor in vascular smooth muscle, suggesting a role in regulating gene expression during arterial responses to injury or hypertension.
Pulver et al. (2004) studied this question. Thapsigargin-induced store-operated Ca2+ entry (SOCE) vs. Inhibition of SOCE (low extracellular Ca2+, 2-APB, Ni2+) was evaluated on CREB phosphorylation, intracellular Ca2+ levels, and c-fos transcription. Depletion of intracellular Ca2+ stores with thapsigargin increased nuclear phospho-CREB levels and c-fos transcription, effects that were abolished by inhibiting store-operated Ca2+ entry.
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