NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals

Juan Antonio Valdés, Jorge Hidalgo, José Luis Galaz, Natalia Puentes, Mónica Silva, Enrique Jaimovich, M. Angélica Carrasco

Resultado de la investigación: Article

33 Citas (Scopus)

Resumen

Depolarization of skeletal muscle cells by either high external K + or repetitive extracellular field potential pulses induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or inositol 1,4,5-trisphosphate (IP3) receptors and show differences in kinetics, amplitude, and subcellular localization. We have reported that the transcriptional regulators including ERKs, cAMP/Ca2+-response element binding protein, c-fos, c-jun, and egr-1 are activated by K+-induced depolarization and that their activation requires IP3-dependent calcium release. We presently describe the activation of the nuclear transcription factor NF-κB in response to depolarization by either high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-κB reporter gene to an intermediate level, whereas long-lasting calcium increases obtained by prolonged electrical stimulation protocols of various frequencies induce maximal activation of NF-κB. This activation is independent of extracellular calcium, whereas calcium release mediated by either ryanodine or IP3 receptors contribute in all conditions tested. NF-κB activation is mediated by IκBα degradation and p65 translocation to the nucleus. Partial blockade by N-acetyl-L-cysteine, a general antioxidant, suggests the participation of reactive oxygen species. Calcium-dependent signaling pathways such as those linked to calcineurin and PKC also contribute to NF-κB activation by depolarization, as assessed by blockade through pharmacological agents. These results suggest that NF-κB activation in skeletal muscle cells is linked to membrane depolarization and depends on the duration of elevated intracellular calcium. It can be regulated by sequential activation of calcium release mediated by the ryanodine and by IP3 receptors.

Idioma originalEnglish
PublicaciónAmerican Journal of Physiology - Cell Physiology
Volumen292
N.º5
DOI
EstadoPublished - may 2007

Huella dactilar

Inositol 1,4,5-Trisphosphate Receptors
Ryanodine Receptor Calcium Release Channel
Muscle Cells
Skeletal Muscle
Calcium
Cyclic AMP Response Element-Binding Protein
Inositol 1,4,5-Trisphosphate
Calcium Signaling
Calcineurin
Acetylcysteine
Reporter Genes
Electric Stimulation
Reactive Oxygen Species
Transcription Factors
Antioxidants
Pharmacology
Membranes

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

Citar esto

Valdés, Juan Antonio ; Hidalgo, Jorge ; Galaz, José Luis ; Puentes, Natalia ; Silva, Mónica ; Jaimovich, Enrique ; Carrasco, M. Angélica. / NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals. En: American Journal of Physiology - Cell Physiology. 2007 ; Vol. 292, N.º 5.
@article{d0417a00f031411486daea5897561a63,
title = "NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals",
abstract = "Depolarization of skeletal muscle cells by either high external K + or repetitive extracellular field potential pulses induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or inositol 1,4,5-trisphosphate (IP3) receptors and show differences in kinetics, amplitude, and subcellular localization. We have reported that the transcriptional regulators including ERKs, cAMP/Ca2+-response element binding protein, c-fos, c-jun, and egr-1 are activated by K+-induced depolarization and that their activation requires IP3-dependent calcium release. We presently describe the activation of the nuclear transcription factor NF-κB in response to depolarization by either high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-κB reporter gene to an intermediate level, whereas long-lasting calcium increases obtained by prolonged electrical stimulation protocols of various frequencies induce maximal activation of NF-κB. This activation is independent of extracellular calcium, whereas calcium release mediated by either ryanodine or IP3 receptors contribute in all conditions tested. NF-κB activation is mediated by IκBα degradation and p65 translocation to the nucleus. Partial blockade by N-acetyl-L-cysteine, a general antioxidant, suggests the participation of reactive oxygen species. Calcium-dependent signaling pathways such as those linked to calcineurin and PKC also contribute to NF-κB activation by depolarization, as assessed by blockade through pharmacological agents. These results suggest that NF-κB activation in skeletal muscle cells is linked to membrane depolarization and depends on the duration of elevated intracellular calcium. It can be regulated by sequential activation of calcium release mediated by the ryanodine and by IP3 receptors.",
keywords = "Electrical stimulation, Intracellular calcium stores, Transcription",
author = "Vald{\'e}s, {Juan Antonio} and Jorge Hidalgo and Galaz, {Jos{\'e} Luis} and Natalia Puentes and M{\'o}nica Silva and Enrique Jaimovich and Carrasco, {M. Ang{\'e}lica}",
year = "2007",
month = "5",
doi = "10.1152/ajpcell.00320.2006",
language = "English",
volume = "292",
journal = "American Journal of Physiology - Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "5",

}

NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals. / Valdés, Juan Antonio; Hidalgo, Jorge; Galaz, José Luis; Puentes, Natalia; Silva, Mónica; Jaimovich, Enrique; Carrasco, M. Angélica.

En: American Journal of Physiology - Cell Physiology, Vol. 292, N.º 5, 05.2007.

Resultado de la investigación: Article

TY - JOUR

T1 - NF-κB activation by depolarization of skeletal muscle cells depends on ryanodine and IP3 receptor-mediated calcium signals

AU - Valdés, Juan Antonio

AU - Hidalgo, Jorge

AU - Galaz, José Luis

AU - Puentes, Natalia

AU - Silva, Mónica

AU - Jaimovich, Enrique

AU - Carrasco, M. Angélica

PY - 2007/5

Y1 - 2007/5

N2 - Depolarization of skeletal muscle cells by either high external K + or repetitive extracellular field potential pulses induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or inositol 1,4,5-trisphosphate (IP3) receptors and show differences in kinetics, amplitude, and subcellular localization. We have reported that the transcriptional regulators including ERKs, cAMP/Ca2+-response element binding protein, c-fos, c-jun, and egr-1 are activated by K+-induced depolarization and that their activation requires IP3-dependent calcium release. We presently describe the activation of the nuclear transcription factor NF-κB in response to depolarization by either high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-κB reporter gene to an intermediate level, whereas long-lasting calcium increases obtained by prolonged electrical stimulation protocols of various frequencies induce maximal activation of NF-κB. This activation is independent of extracellular calcium, whereas calcium release mediated by either ryanodine or IP3 receptors contribute in all conditions tested. NF-κB activation is mediated by IκBα degradation and p65 translocation to the nucleus. Partial blockade by N-acetyl-L-cysteine, a general antioxidant, suggests the participation of reactive oxygen species. Calcium-dependent signaling pathways such as those linked to calcineurin and PKC also contribute to NF-κB activation by depolarization, as assessed by blockade through pharmacological agents. These results suggest that NF-κB activation in skeletal muscle cells is linked to membrane depolarization and depends on the duration of elevated intracellular calcium. It can be regulated by sequential activation of calcium release mediated by the ryanodine and by IP3 receptors.

AB - Depolarization of skeletal muscle cells by either high external K + or repetitive extracellular field potential pulses induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or inositol 1,4,5-trisphosphate (IP3) receptors and show differences in kinetics, amplitude, and subcellular localization. We have reported that the transcriptional regulators including ERKs, cAMP/Ca2+-response element binding protein, c-fos, c-jun, and egr-1 are activated by K+-induced depolarization and that their activation requires IP3-dependent calcium release. We presently describe the activation of the nuclear transcription factor NF-κB in response to depolarization by either high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-κB reporter gene to an intermediate level, whereas long-lasting calcium increases obtained by prolonged electrical stimulation protocols of various frequencies induce maximal activation of NF-κB. This activation is independent of extracellular calcium, whereas calcium release mediated by either ryanodine or IP3 receptors contribute in all conditions tested. NF-κB activation is mediated by IκBα degradation and p65 translocation to the nucleus. Partial blockade by N-acetyl-L-cysteine, a general antioxidant, suggests the participation of reactive oxygen species. Calcium-dependent signaling pathways such as those linked to calcineurin and PKC also contribute to NF-κB activation by depolarization, as assessed by blockade through pharmacological agents. These results suggest that NF-κB activation in skeletal muscle cells is linked to membrane depolarization and depends on the duration of elevated intracellular calcium. It can be regulated by sequential activation of calcium release mediated by the ryanodine and by IP3 receptors.

KW - Electrical stimulation

KW - Intracellular calcium stores

KW - Transcription

UR - http://www.scopus.com/inward/record.url?scp=34250635494&partnerID=8YFLogxK

U2 - 10.1152/ajpcell.00320.2006

DO - 10.1152/ajpcell.00320.2006

M3 - Article

C2 - 17215326

AN - SCOPUS:34250635494

VL - 292

JO - American Journal of Physiology - Cell Physiology

JF - American Journal of Physiology - Cell Physiology

SN - 0363-6143

IS - 5

ER -