scholarly journals Effects of acetylcholine and electrical stimulation on glial cell line-derived neurotrophic factor production in skeletal muscle cells

2014 ◽  
Vol 1588 ◽  
pp. 47-54 ◽  
Author(s):  
John-Mary Vianney ◽  
Damon A. Miller ◽  
John M. Spitsbergen
Nature ◽  
1979 ◽  
Vol 281 (5732) ◽  
pp. 586-588 ◽  
Author(s):  
Vanda A. Lennon ◽  
Susan Peterson ◽  
David Schubert

Author(s):  
Hidenori Suzuki ◽  
Asako Hase ◽  
Yuhei Miyata ◽  
Kiichi Arahata ◽  
Chihiro Akazawa

2002 ◽  
Vol 454 (3) ◽  
pp. 350-360 ◽  
Author(s):  
Sho Kanzaki ◽  
Timo Stöver ◽  
Kohei Kawamoto ◽  
Diane M. Prieskorn ◽  
Richard A. Altschuler ◽  
...  

2004 ◽  
Vol 68 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Yutaka Koyama ◽  
Hiroaki Egawa ◽  
Masakazu Osakada ◽  
Akemichi Baba ◽  
Toshio Matsuda

Cell Research ◽  
2008 ◽  
Vol 18 (S1) ◽  
pp. S85-S85
Author(s):  
Li-ye Yang ◽  
Qiang Chen ◽  
Tian-hua Huang ◽  
Wenyu Li ◽  
Jia-kun Zheng ◽  
...  

2008 ◽  
Vol 294 (3) ◽  
pp. C715-C725 ◽  
Author(s):  
Juan Antonio Valdés ◽  
Eduardo Gaggero ◽  
Jorge Hidalgo ◽  
Nancy Leal ◽  
Enrique Jaimovich ◽  
...  

Depolarization of skeletal muscle cells triggers intracellular Ca2+ signals mediated by ryanodine and inositol 1,4,5-trisphosphate (IP3) receptors. Previously, we have reported that K+-induced depolarization activates transcriptional regulators ERK, cAMP response element-binding protein, c- fos, c- jun, and egr-1 through IP3-dependent Ca2+ release, whereas NF-κB activation is elicited by both ryanodine and IP3 receptor-mediated Ca2+ signals. We have further shown that field stimulation with electrical pulses results in an NF-κB activation increase dependent of the amount of pulses and independent of their frequency. In this work, we report the results obtained for nuclear factor of activated T cells (NFAT)-mediated transcription and translocation generated by both K+ and electrical stimulation protocols in primary skeletal muscle cells and C2C12 cells. The Ca2+ source for NFAT activation is through release by ryanodine receptors and extracellular Ca2+ entry. We found this activation to be independent of the number of pulses within a physiological range of stimulus frequency and enhanced by long-lasting low-frequency stimulation. Therefore, activation of the NFAT signaling pathway differs from that of NF-κB and other transcription factors. Calcineurin enzyme activity correlated well with the relative activation of NFAT translocation and transcription using different stimulation protocols. Furthermore, both K+-induced depolarization and electrical stimulation increased mRNA levels of the type 1 IP3 receptor mediated by calcineurin activity, which suggests that depolarization may regulate IP3 receptor transcription. These results confirm the presence of at least two independent pathways for excitation-transcription coupling in skeletal muscle cells, both dependent on Ca2+ release and triggered by the same voltage sensor but activating different intracellular release channels.


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