Regulation of Ca<inf>V</inf>3.1 channels by glucocorticoids

Traudy Avila, Oscar Hernández-Hernández, Angélica Almanza, Mario Bermúdez De León, Mercedes Urban, Enrique Soto, Bulmaro Cisneros, Ricardo Felix

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)1265-1273
Number of pages9
JournalCellular and Molecular Neurobiology
DOIs
Publication statusPublished - 1 Dec 2009
Externally publishedYes

Fingerprint

Glucocorticoids
Western Blotting
Biotinylation
HEK293 Cells
Neurotransmitter Agents
Real-Time Polymerase Chain Reaction
Cell Membrane
Hormones
Polymerase Chain Reaction
Messenger RNA
Proteins

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

Cite this

Avila, T., Hernández-Hernández, O., Almanza, A., Bermúdez De León, M., Urban, M., Soto, E., ... Felix, R. (2009). Regulation of Ca<inf>V</inf>3.1 channels by glucocorticoids. Cellular and Molecular Neurobiology, 1265-1273. https://doi.org/10.1007/s10571-009-9422-2
Avila, Traudy ; Hernández-Hernández, Oscar ; Almanza, Angélica ; Bermúdez De León, Mario ; Urban, Mercedes ; Soto, Enrique ; Cisneros, Bulmaro ; Felix, Ricardo. / Regulation of Ca<inf>V</inf>3.1 channels by glucocorticoids. In: Cellular and Molecular Neurobiology. 2009 ; pp. 1265-1273.
@article{2c090a2997674f9a9622ee1e430829b2,
title = "Regulation of CaV3.1 channels by glucocorticoids",
abstract = "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. {\circledC} 2009 Springer Science+Business Media, LLC.",
author = "Traudy Avila and Oscar Hern{\'a}ndez-Hern{\'a}ndez and Ang{\'e}lica Almanza and {Berm{\'u}dez De Le{\'o}n}, Mario and Mercedes Urban and Enrique Soto and Bulmaro Cisneros and Ricardo Felix",
year = "2009",
month = "12",
day = "1",
doi = "10.1007/s10571-009-9422-2",
language = "English",
pages = "1265--1273",
journal = "Cellular and Molecular Neurobiology",
issn = "0272-4340",
publisher = "Springer New York",

}

Avila, T, Hernández-Hernández, O, Almanza, A, Bermúdez De León, M, Urban, M, Soto, E, Cisneros, B & Felix, R 2009, 'Regulation of Ca<inf>V</inf>3.1 channels by glucocorticoids', Cellular and Molecular Neurobiology, pp. 1265-1273. https://doi.org/10.1007/s10571-009-9422-2

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 journalArticle

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 -