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1 Centro FONDAP de Estudios Moleculares de la Celula, Facultad de Medicina, Universidad de Chile, Santiago, Chile
2 Centro FONDAP de Estudios Moleculares de la Celula, Facultad de Medicina, Universidad de Chile, Santiago, Chile; Programa de Fisiologia y Biofisica, Instituto de Ciencias Biomedicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile
3 Programa de Biologia Celular y Molecular, Instituto de Ciencias Biomedicas,Facultad de Medicina, Universidad de Chile, Santiago, Chile; Centro FONDAP de Estudios Moleculares de la Celula, Facultad de Medicina, Universidad de Chile, Santiago, Chile
* To whom correspondence should be addressed. E-mail: mcarras{at}med.uchile.cl.
Depolarization of skeletal muscle cells either by high external K+ or by repetitive extracellular field potential pulses, induces calcium release from internal stores. The two components of this release are mediated by either ryanodine receptors or IP3 receptors and show differences in kinetics, amplitude and subcellular localization. We have reported that the activation of the transcriptional regulators ERKs, CREB, c-fos, c-jun and egr-1 by K+ -induced depolarization requires IP3-dependent calcium release. We now describe the activation of the nuclear transcription factor NF-
B in response to depolarization either by high K+ (chronic) or electrical pulses (fluctuating). Calcium transients of relative short duration activate an NF-B reporter gene to an intermediate level while long lasting calcium increase obtained by prolonged electrical stimulation protocols of various frequencies induce maximal activation of NF-B. This activation is independent of extracellular calcium, whilst calcium release mediated by either ryanodine receptors or IP3 receptors contribute in all conditions tested. NF-B activation is mediated by IB
degradation and p65 translocation to the nucleus. Partial blockade by N-acetylcysteine, a general antioxidant, suggests the participation of reactive oxygen species. Calcium sensors signaling pathways such as those linked to calcineurin and PKC also contribute to NF-B activation by depolarization, as assessed by blockade through pharmacological agents. These results suggest that NF-B 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 receptors and by IP3 receptors.
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