Inhibition of ryanodine receptor 1 in fast skeletal muscle fibers induces a fast-to-slow muscle fiber type transition

Jordan, Theresa; Jiang, Hongbin; Li, Hui; DiMario, Joseph X.

doi:10.1242/jcs.01543

Cited by 31 publications

(28 citation statements)

References 39 publications

(64 reference statements)

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“…K ϩ -depolarized C2C12 cells present the same dependence, with an important role for extracellular Ca 2ϩ as well (32). Other studies, performed in C2C12 cells and cultured avian skeletal muscle fibers, have reported a role for both RyR and IP 3 R-mediated Ca 2ϩ release in NFAT activation (20,21,35).…”

mentioning

confidence: 63%

“…A mutagenesis study (19) has indicated that both NFAT and MEF2 binding sites are required for innervation-induced MyHC2 promoter activity in slow muscle fibers. Basically, there is NFAT activation by RyR inhibition (20), whereas IP3R blockade results in the opposite effect (21). These results might reflect complex mechanisms of NFAT regulation in another developmental stage as well as differences with respect to the stimulatory pattern used.…”

Section: Discussionmentioning

confidence: 99%

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NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

Valdés¹,

Gaggero²,

Hidalgo³

et al. 2008

American Journal of Physiology-Cell Physiology

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. NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells. Am J Physiol Cell Physiol 294: C715-C725, 2008. First published January 9, 2008 doi:10.1152/ajpcell.00195.2007.-Depolarization of skeletal muscle cells triggers intracellular Ca 2ϩ signals mediated by ryanodine and inositol 1,4,5-trisphosphate (IP3) receptors. Previously, we have reported that K ϩ -induced depolarization activates transcriptional regulators ERK, cAMP response element-binding protein, c-fos, c-jun, and egr-1 through IP3-dependent Ca 2ϩ release, whereas NF-B activation is elicited by both ryanodine and IP3 receptor-mediated Ca 2ϩ signals. We have further shown that field stimulation with electrical pulses results in an NF-B 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 ϩ and electrical stimulation protocols in primary skeletal muscle cells and C2C12 cells. The Ca 2ϩ source for NFAT activation is through release by ryanodine receptors and extracellular Ca 2ϩ 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-B 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 ϩ -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 excitationtranscription coupling in skeletal muscle cells, both dependent on Ca 2ϩ release and triggered by the same voltage sensor but activating different intracellular release channels. nuclear factor of activated T cells transcription; nuclear factor of activated T cells translocation; calcineurin; inositol 1,4,5-trisphosphate receptor; ryanodine receptor IN SKELETAL MUSCLE CELLS, depolarization by high K ϩ induces Ca 2ϩ release from intracellular stores mediated both by ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs) (11,18). The kinetics of the resulting Ca 2ϩ

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mentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

Valdés¹,

Gaggero²,

Hidalgo³

et al. 2008

American Journal of Physiology-Cell Physiology

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“…In adult muscles, dystrophin and α-syntrophin regulate PLC activity by stabilizing the sarcolemma; thus, dystrophin absence leads to increased PLC activity (Jordan et al, 2004;Mondin et al, 2009;Sabourin et al, 2012). Furthermore, previous studies showed that dystrophic human samples and murine cell lines expressed high levels of IP3 compared with normal cell lines (Liberona et al, 1998;Mondin et al, 2009) and IP3-induced Ca 2+ release altered gene expression regulation (Powell et al, 2001;Araya et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ signaling mediates delayed myogenesis in Duchenne muscular dystrophy fetal muscle

et al. 2016

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Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disorder characterized by muscle wasting and premature death. The defective gene is dystrophin, a structural protein, absence of which causes membrane fragility and myofiber necrosis. Several lines of evidence showed that in adult DMD patients dystrophin is involved in signaling pathways that regulate calcium homeostasis and differentiation programs. However, secondary aspects of the disease, such as inflammation and fibrosis development, might represent a bias in the analysis. Because fetal muscle is not influenced by gravity and does not suffer from mechanical load and/or inflammation, we investigated 12-week-old fetal DMD skeletal muscles, highlighting for the first time early alterations in signaling pathways mediated by the absence of dystrophin itself. We found that PLC/IP3/IP3R/Ryr1/Ca 2+ signaling is widely active in fetal DMD skeletal muscles and, through the calcium-dependent PKCα protein, exerts a fundamental regulatory role in delaying myogenesis and in myofiber commitment. These data provide new insights into the origin of DMD pathology during muscle development.

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“…RyR1 inhibition increases slow MyHC2 promoter activity in innervated pectoralis major (PM) muscle fibers, enhances the D r a f t transcriptional activity of nuclear factor of activated T cells and myocyte enhancer factor 2, and enhances their interactions with their respective binding sites on the slow MyHC2 promoter; these results reveal that RyR1 activity in innervated fast PM muscle fibers contributes to cell type-specific repression (Jordan et al 2004). ERBB4 is a receptor for neuregulins that belongs to a family of closely related proteins implicated as regulators of neural and muscle development and the differentiation and oncogenic transformation of mammary epithelia (Carraway and Burden 1995;Plowman et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Sequencing and characterization of lncRNAs in the breast muscle of Gushi and Arbor Acres chickens

Ren

et al. 2018

Genome

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Chicken muscle quality is one of the most important factors determining the economic value of poultry, and muscle development and growth are affected by genetics, environment, and nutrition. However, little is known about the molecular regulatory mechanisms of long non-coding RNAs (lncRNAs) in chicken skeletal muscle development. Our study aimed to better understand muscle development in chickens and thereby improve meat quality. In this study, Ribo-Zero RNA-Seq was used to investigate differences in the expression profiles of muscle development related genes and associated pathways between Gushi (GS) and Arbor Acres (AA) chickens. We identified two muscle tissue specific expression lncRNAs. In addition, the target genes of these lncRNAs were significantly enriched in certain biological processes and molecular functions, as demonstrated by Gene Ontology (GO) analysis, and these target genes participate in five signaling pathway, as revealed by an analysis of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Taken together, these data suggest that different lncRNAs might be involved in regulating chicken muscle development and growth and provide new insight into the molecular mechanisms of lncRNAs.

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Inhibition of ryanodine receptor 1 in fast skeletal muscle fibers induces a fast-to-slow muscle fiber type transition

Cited by 31 publications

References 39 publications

NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

NFAT activation by membrane potential follows a calcium pathway distinct from other activity-related transcription factors in skeletal muscle cells

Inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ signaling mediates delayed myogenesis in Duchenne muscular dystrophy fetal muscle

Sequencing and characterization of lncRNAs in the breast muscle of Gushi and Arbor Acres chickens

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