The activity of low voltage-activated Ca(2+) (Ca(V)3) channels is tightly coupled to neurotransmitter and hormone secretion. Previous studies have shown that Ca(V)3 channels are regulated by glucocorticoids (GCs), though the mechanism underlying channel regulation remains unclear. Here, using the pituitary GH(3) cell line as a model, we investigated whether Ca(V)3 channel expression is under the control of GCs, and if their actions are mediated by transcriptional and/or post-transcriptional mechanisms.
View Article and Find Full Text PDFSingle non-confluent MDCK cells respond immediately to a sharp decrease in extracellular Ca2+ (< or = 5 microM) with an intense reversible retraction, along with an increase in cell height, correlating in overall rate and extent with initial cell size. Optical sectioning of individual cells by confocal microscopy showed that this structural response, observed in about 50% of the population, involves narrowing and even furrowing near the base of the cell by a thickened peripheral belt of actin filaments, which remains associated with the cortex instead of being internalized in the cytoplasm. Single cells retracted significantly in response to low Ca2+ under conditions that have been found largely inhibitory for retraction of confluent cells, such as Ca2+ replacement with Ba2+ and the substitution of Na+ with choline, a non-permeant cation.
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