Changes in IP3 Metabolism During Skeletal Muscle Development In Vivo and In Vitro

Carrasco, M. Angélica; Marambio, Paola; Jaimovich, Enrique

doi:10.1016/s0305-0491(96)00244-1

Cited by 16 publications

(8 citation statements)

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“…A fairly elevated mass of resting IP 3 seems characteristic both for adult muscle 14,27 and for cultured muscle cells 5 ; nevertheless, when we compare normal and dystrophic cell lines, we see that the basal levels of IP 3 ranged between 10 and 60 pmol/mg protein in normal cells, but dystrophic cells have basal IP 3 levels two-to threefold higher than their normal counterparts. These figures do not vary significantly when results are calculated either per µmol of membrane cholesterol or per million of cells, meaning that these IP 3 mass differences are not a consequence of altered cell composition.…”

Section: Discussionmentioning

confidence: 69%

Differences in both inositol 1,4,5-trisphosphate mass and inositol 1,4,5-trisphosphate receptors between normal and dystrophic skeletal muscle cell lines

Liberona¹,

Powell²,

Shenoi³

et al. 1998

Muscle Nerve

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Human normal (RCMH) and Duchenne muscular dystrophy (RCDMD) cell lines, as well as newly developed normal and dystrophic murine cell lines, were used for the study of both changes in inositol 1,4,5‐trisphosphate (IP3) mass and IP3 binding to receptors. Basal levels of IP3 were increased two‐ to threefold in dystrophic human and murine cell lines compared to normal cell lines. Potassium depolarization induced a time‐dependent IP3 rise in normal human cells and cells of the myogenic mouse cell line (129CB3), which returned to their basal levels after 60 s. However, in the human dystrophic cell line (RCDMD), IP3 levels remained high up to 200 s after potassium depolarization. Expression of IP3 receptors was studied measuring specific binding of 3H‐IP3 in the murine cell lines (normal 129CB3 and dystrophic mdx XLT 4‐2). All the cell lines bind 3H‐IP3 with relatively high affinity (Kd: between 40 and 100 nmol/L). IP3 receptors are concentrated in the nuclear fraction, and their density is significantly higher in dystrophic cells compared to normal. These findings together with high basal levels of IP3 mass suggest a possible role for this system in the deficiency of intracellular calcium regulation in Duchenne muscular dystrophy. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:902–909, 1998.

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Section: Discussionmentioning

confidence: 69%

Differences in both inositol 1,4,5-trisphosphate mass and inositol 1,4,5-trisphosphate receptors between normal and dystrophic skeletal muscle cell lines

Liberona¹,

Powell²,

Shenoi³

et al. 1998

Muscle Nerve

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“…Skeletal muscle fibers have been shown to possess the basic biochemical machinery for generation and catabolism of inositol phosphates (7,14,16,28), and cultured myotubes have IP 3 receptors associated with cell nuclei (17). Nevertheless, neither the role nor the regulation of this second messenger pathway has been elucidated in this tissue.…”

mentioning

confidence: 99%

“…Little is known about the steroid hormone effects in skeletal muscle, and the fast effects of gonadal steroids (progesterone, estradiol, and testosterone) or adrenal steroids (glucocorticoids and mineralocorticoids) on muscle cells have not been described; neither has a clear role for steroid hormones during muscle development been demonstrated. Skeletal muscle myoblasts are the precursors to skeletal muscle fibers, and during the differentiation process they fuse into multinucleated myotubes that express many skeletal muscle-specific markers (7,17). Thus we have chosen to study the early effects of different steroid hormones on [Ca 2ϩ ] i levels in skeletal muscle cell cultures, analyzing both the spatial and the time distributions of these signals, as well as any possible relation with intracellular IP 3 concentration.…”

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confidence: 99%

Aldosterone- and testosterone-mediated intracellular calcium response in skeletal muscle cell cultures

Estrada

Liberona

Miranda

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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] i was monitored in Fluo 3-acetoxymethyl esterloaded myotubes by either confocal microscopy or fluorescence microscopy, with the use of out-of-focus fluorescence elimination. The mass of IP 3 was determined by radioreceptor displacement assay. [Ca 2ϩ ] i changes after either aldosterone (10-100 nM) or testosterone (50-100 nM) were observed; a relatively fast (Ͻ2 min) calcium transient, frequently accompanied by oscillations, was evident with both hormones. A slow rise in [Ca 2ϩ ] i that reached its maximum after a 30-min exposure to aldosterone was also observed. Calcium responses seem to be fairly specific for aldosterone and testosterone, because several other steroid hormones do not induce detectable changes in fluorescence, even at 100-fold higher concentrations. The mass of IP 3 increased transiently to reach two-to threefold the basal level 45 s after addition of either aldosterone or testosterone, and the IP 3 transient was more rapid than the fast calcium signal. Spironolactone, an inhibitor of the intracellular aldosterone receptor, or cyproterone acetate, an inhibitor of the testosterone receptor, had no effect on the fast [Ca 2ϩ ] i signal or in the increase in IP 3 mass. These signals could mean that there are distinct nongenomic pathways for the action of these two steroids in skeletal muscle cells. steroid hormones; inositol 1,4,5-trisphosphate; calcium waves; nongenomic pathway STEROID HORMONES ARE CAPABLE of producing rapid (within 2 min) effects in several cell types (12,22,36). These rapid responses are not compatible with the classical mechanism of action proposed for these hormones, which involves binding to intracellular receptors, transcriptional processes, and protein synthesis (1, 20). Thus, for rapid steroid effects, the existence of membrane receptors for steroids has been proposed (2, 37). In skeletal muscle, steroid hormones have long been known to modulate gene expression, and hormones like testosterone have been related to both muscle hypertrophy (4, 25) and upregulation of a number of proteins (31). In particular, glucocorticoids and mineralocorticoids have been related to up-and downregulation, respectively, of sodium pumps in skeletal muscle (10), implying the presence of steroid hormone receptors in muscle cells. Because all these effects have been the result of chronic (hours to days) treatments, it would be interesting to know whether exposure to these hormones is also accompanied by fast nongenomic events.The signal transduction mechanism for the rapid action of steroids in some cellular models could be regulated by second messengers such as intracellular calcium ([Ca 2ϩ

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“…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). In addition, it was determined that modifications in the metabolism of IP3 were fundamental at different stages of muscle development (Carrasco et al, 1997), and others suggested a role for IP3/IP3R during skeletal myocyte development (Rosemblit et al, 1999) and in cardiomyocyte hypertrophy (Arantes et al, 2012). Therefore, we investigated IP3R and IP3 pathway, demonstrating their overactivity in fetal DMD muscle.…”

Section: Discussionmentioning

confidence: 99%

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

Farini¹,

Sitzia²,

Cassinelli³

et al. 2016

Journal of Cell Science

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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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Changes in IP3 Metabolism During Skeletal Muscle Development In Vivo and In Vitro

Cited by 16 publications

References 50 publications

Differences in both inositol 1,4,5-trisphosphate mass and inositol 1,4,5-trisphosphate receptors between normal and dystrophic skeletal muscle cell lines

Differences in both inositol 1,4,5-trisphosphate mass and inositol 1,4,5-trisphosphate receptors between normal and dystrophic skeletal muscle cell lines

Aldosterone- and testosterone-mediated intracellular calcium response in skeletal muscle cell cultures

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

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