Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1265-1273 |
| Number of pages | 9 |
| Journal | Cellular and Molecular Neurobiology |
| DOIs | |
| Publication status | Published - 1 Dec 2009 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience
- Cell Biology
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Regulation of Ca<inf>V</inf>3.1 channels by glucocorticoids. / Avila, Traudy; Hernández-Hernández, Oscar; Almanza, Angélica; Bermúdez De León, Mario; Urban, Mercedes; Soto, Enrique; Cisneros, Bulmaro; Felix, Ricardo.
In: Cellular and Molecular Neurobiology, 01.12.2009, p. 1265-1273.Research output: Contribution to journal › Article
TY - JOUR
T1 - Regulation of CaV3.1 channels by glucocorticoids
AU - Avila, Traudy
AU - Hernández-Hernández, Oscar
AU - Almanza, Angélica
AU - Bermúdez De León, Mario
AU - Urban, Mercedes
AU - Soto, Enrique
AU - Cisneros, Bulmaro
AU - Felix, Ricardo
PY - 2009/12/1
Y1 - 2009/12/1
N2 - The activity of low voltage-activated Ca2+(CaV3) channels is tightly coupled to neurotransmitter and hormone secretion. Previous studies have shown that CaV3 channels are regulated by glucocorticoids (GCs), though the mechanism underlying channel regulation remains unclear. Here, using the pituitary GH3cell line as a model, we investigated whether CaV3 channel expression is under the control of GCs, and if their actions are mediated by transcriptional and/or post-transcriptional mechanisms. RT-PCR and western blot analyses showed that CaV3.1 but not CaV3.2 and CaV3.3 channels is expressed in the GH3cells, and patch clamp recordings confirmed that Ca2+currents through low voltage-activated channels were decreased after chronic treatment with GCs. Consistent with this, total plasma membrane expression of CaV3.1 protein as analyzed by cell-surface biotinylation assays and semi-quantitative western blotting was also down-regulated, while quantitative real-time RT-PCR analysis revealed a significant decrease of CaV3.1 mRNA expression in the treated cells. In contrast, patch-clamp recordings on HEK-293 cells stably expressing recombinant CaV3.1 channels showed that Ca2+currents were not affected by GC treatment. These results suggest that decreased transcription is a likely mechanism to explain the inhibitory actions of GCs on the functional expression of native CaV3.1 channels. © 2009 Springer Science+Business Media, LLC.
AB - The activity of low voltage-activated Ca2+(CaV3) channels is tightly coupled to neurotransmitter and hormone secretion. Previous studies have shown that CaV3 channels are regulated by glucocorticoids (GCs), though the mechanism underlying channel regulation remains unclear. Here, using the pituitary GH3cell line as a model, we investigated whether CaV3 channel expression is under the control of GCs, and if their actions are mediated by transcriptional and/or post-transcriptional mechanisms. RT-PCR and western blot analyses showed that CaV3.1 but not CaV3.2 and CaV3.3 channels is expressed in the GH3cells, and patch clamp recordings confirmed that Ca2+currents through low voltage-activated channels were decreased after chronic treatment with GCs. Consistent with this, total plasma membrane expression of CaV3.1 protein as analyzed by cell-surface biotinylation assays and semi-quantitative western blotting was also down-regulated, while quantitative real-time RT-PCR analysis revealed a significant decrease of CaV3.1 mRNA expression in the treated cells. In contrast, patch-clamp recordings on HEK-293 cells stably expressing recombinant CaV3.1 channels showed that Ca2+currents were not affected by GC treatment. These results suggest that decreased transcription is a likely mechanism to explain the inhibitory actions of GCs on the functional expression of native CaV3.1 channels. © 2009 Springer Science+Business Media, LLC.
U2 - 10.1007/s10571-009-9422-2
DO - 10.1007/s10571-009-9422-2
M3 - Article
SP - 1265
EP - 1273
JO - Cellular and Molecular Neurobiology
JF - Cellular and Molecular Neurobiology
SN - 0272-4340
ER -