Low-pH preparation of skeletal muscle satellite cells can be used to study activation in vitro

Tatsumi, Ryuichi; Yamada, Michiko; Katsuki, Yoshitaka; Okamoto, Shinpei; Ishizaki, Junji; Mizunoya, Wataru; Ikeuchi, Yoshihide; Hattori, Akihito; Shimokawa, Hiroaki; Allen, Ronald E.

doi:10.1016/j.biocel.2006.04.003

Cited by 29 publications

(34 citation statements)

References 20 publications

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“…In previous experiments, it was demonstrated with isolated satellite cells that entry into the cell cycle is accelerated in vitro by treatment with HGF (1), NO donors (3,5,(23)(24)(25), and by mechanical stretch (21,28,31,32). It has been shown subsequently that these stimuli activate quiescent satellite cells in vivo (27) through the release of HGF from the extracellular matrix and its interaction with the c-met receptor.…”

Section: Resultsmentioning

confidence: 99%

“…The intracellular signaling receptor for HGF is the c-met proto-oncogene, and its message and protein have been found in quiescent and activated satellite cells (1,8,20). Thus release of HGF from its sequestration and subsequent presentation to the c-met receptor may be a critical aspect of the activation of quiescent satellite cells.In previous works, we employed a FlexerCell system (Flexcell International, McKeesport, PA) to apply cyclic stretch to isolated rat satellite cells and found that mechanical stretch triggers satellite cell activation by releasing HGF from its tethering in the extracellular matrix (21,23,26,28). This phenomenon is relevant to satellite cells in living skeletal muscle as revealed by an in vivo muscle stretch model (16,27).…”

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confidence: 99%

“…In previous works, we employed a FlexerCell system (Flexcell International, McKeesport, PA) to apply cyclic stretch to isolated rat satellite cells and found that mechanical stretch triggers satellite cell activation by releasing HGF from its tethering in the extracellular matrix (21,23,26,28). This phenomenon is relevant to satellite cells in living skeletal muscle as revealed by an in vivo muscle stretch model (16,27).…”

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confidence: 99%

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A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation

Tatsumi¹,

Wuollet²,

Tabata³

et al. 2009

American Journal of Physiology-Cell Physiology

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RE.A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation. Am J Physiol Cell Physiol 296: C922-C929, 2009. First published January 21, 2009 doi:10.1152/ajpcell.00471.2008.-When skeletal muscle is stretched or injured, myogenic satellite cells are activated to enter the cell cycle. This process depends on nitric oxide (NO) production by NO synthase (NOS), matrix metalloproteinase activation, release of hepatocyte growth factor (HGF) from the extracellular matrix, and presentation of HGF to the c-met receptor as demonstrated by a primary culture and in vivo assays. We now add evidence that calcium-calmodulin is involved in the satellite cell activation cascade in vitro. Conditioned medium from cultures that were treated with a calcium ionophore (A23187, ionomycin) for 2 h activated cultured satellite cells and contained active HGF, similar to the effect of mechanical stretch or NO donor treatments. The response was abolished by addition of calmodulin inhibitors (calmidazolium, W-13, W-12) or a NOS inhibitor N G -nitro-L-arginine methyl ester hydrochloride but not by its less inactive enantiomer N G -nitro-Darginine methyl ester hydrochloride. Satellite cells were also shown to express functional calmodulin protein having a calcium-binding activity at 12 h postplating, which is the time at which the calcium ionophore was added in this study and the stretch treatment was applied in our previous experiments. Therefore, results from these experiments provide an additional insight that calcium-calmodulin mediates HGF release from the matrix and that this step in the activation pathway is upstream from NO synthesis. muscle regeneration; stretch-activation SKELETAL MUSCLE SATELLITE cells are resident myogenic stem cells normally found in a quiescent state in adult skeletal muscles. When muscle is injured, overused, or mechanically stretched, these cells are activated to enter the cell cycle, divide, differentiate, and fuse with muscle fibers to repair damaged regions and to enhance hypertrophy of muscle fibers (reviewed in Refs. 7,10,17). Therefore, mechanical changes in muscle can initiate events that lead to satellite cell activation, although the mechanism has not been clearly delineated.Of all growth factors studied thus far, only hepatocyte growth factor (HGF) provides a signal that can activate quiescent satellite cells in primary culture and in vivo (1,20). HGF is a heparin-binding protein localized in the extracellular domain of uninjured skeletal muscle fibers, and its predominant form is the active heterodimer of the 60-kDa ␣-chain and 30-kDa ␤-chain (25). The intracellular signaling receptor for HGF is the c-met proto-oncogene, and its message and protein have been found in quiescent and activated satellite cells (1,8,20). Thus release of HGF from its sequestration and subsequent presentation to the c-met receptor may be a critical aspect of the activation of quiescent satellite cells.In previous works, we employed a FlexerCell system (Flexcell Int...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation

Tatsumi¹,

Wuollet²,

Tabata³

et al. 2009

American Journal of Physiology-Cell Physiology

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“…A mononuclear-cell preparation of intramuscular activated macrophages and myoblasts was obtained from TA muscles 5 days after CTX injection, according to a conventional satellite cell/myoblast isolation procedure (Allen et al 1997;Tatsumi et al 2006) with a slight modification (Sakaguchi et al, in press). Cells were maintained on Nunc Lab-Tek chamberslides (177445JP; Thermo Fisher Scientific, Waltham, MA, USA) for 24 h in Dulbecco's modified Eagle's medium (DMEM; 31600-034 from Invitrogen, Grand Island, NY, USA) containing 10% normal horse serum (HS; 16050-122), 1% antibiotic-antimycotic mixture (15240-062) and 0.5% gentamicin (15710-064) (10% HS-DMEM, pH 7.2) in a humidified atmosphere of 5% CO2 at 37°C.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Supplementary immunocytochemistry of hepatocyte growth factor production in activated macrophages early in muscle regeneration

Sawano

Suzuki

et al. 2014

Animal Science Journal

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Regenerative intramuscular motor-innervation is thought to reside in the spatiotemporal expression of axon-guidance molecules. Our previous studies showed that resident myogenic stem cells, satellite cells, up-regulate a secreted neural-chemorepellent semaphorin 3A (Sema3A) during the early-differentiation period, in response to hepatocyte growth factor (HGF) elevated in injured muscle. However, a paracrine source of the HGF release is still unknown. Very recently, we proposed a possible contribution of anti-inflammatory macrophages (CD206-positive M2) by showing that M2 cells infiltrate predominantly at the early-differentiation phase (3-5 days post-injury) and produce/secrete large amounts of HGF. However, in understanding this concept there still remains a critical need to examine if phagocytotic pro-inflammatory macrophages (CD86-positive M1), another activated-phenotype still present at the early-differentiation phase concerned, produce HGF upon muscle injury. The current immunocytochemical study demonstrated that the HGF expression is negative for M1 prepared from cardiotoxin-injured Tibialis anterior muscle at day 5, in contrast to the intense fluorescent-signal of M2 served as a positive control. This supplementary result advances our understanding of a spatiotemporal burst of HGF secretion from M2 populations (not M1) to impact Sema3A expression, which ensures a coordinated delay in attachment of motoneuron terminals onto damaged and generating fibers during the early phase of muscle regeneration.

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“…HGF is a potent mitogen, motogen, and morphogen for a wide variety of epithelial cells and tissues, as well as in melanocytes and endothelial and hematopoietic cells. HGF is present in the saline extract of lightly crushed muscle tissue that is used to model diffusible factors derived from experimental muscle injury that may function in muscle regeneration (7,9,11,52) and functions as an essential cue for muscle fiber growth and regeneration by stimulating satellite cell activation and proliferation upon mechanical insult or perturbation of muscle tissue (53)(54)(55)(56)(57)(58)61; reviewed in Refs. 59 and 62).…”

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Growth factor regulation of neural chemorepellent Sema3A expression in satellite cell cultures

Mai-Khoi

Sato

Shimizu

et al. 2011

American Journal of Physiology-Cell Physiology

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Successful regeneration and remodeling of the intramuscular motoneuron network and neuromuscular connections are critical for restoring skeletal muscle function and physiological properties. The regulatory signals of such coordination remain unclear, although axon-guidance molecules may be involved. Recently, satellite cells, resident myogenic stem cells positioned beneath the basal lamina and at high density at the myoneural junction regions of mature fibers, were shown to upregulate a secreted neural chemorepellent semaphorin 3A (Sema3A) in response to in vivo muscle-crush injury. The initial report on that expression centered on the observation that hepatocyte growth factor (HGF), an essential cue in muscle fiber growth and regeneration, remarkably upregulates Sema3A expression in early differentiated satellite cells in vitro [Tatsumi et al., Am J Physiol Cell Physiol 297: C238-C252, 2009]. Here, we address regulatory effects of basic fibroblast growth factor (FGF2) and transforming growth factor (TGF)-βs on Sema3A expression in satellite cell cultures. When treated with FGF2, Sema3A message and protein were upregulated as revealed by reverse transcription-polymerase chain reaction and immunochemical studies. Sema3A upregulation by FGF2 was dose dependent with a maximum (8- to 1-fold relative to the control) at 2.5 ng/ml (150 pM) and occurred exclusively at the early differentiation stage. The response was highly comparable in dose response and timing to effects of HGF treatment, without any additive or synergistic effect from treatment with a combination of both potent upregulators. In contrast, TGF-β2 and -β3 potently decreased basal Sema3A expression; the maximum effect was at very low concentrations (40 and 8 pM, respectively) and completely cancelled the activities of FGF2 and HGF to upregulate Sema3A. These results therefore encourage the prospect that a time-coordinated increase in HGF, FGF2, and TGF-β ligands and their receptors promotes a programmed strategy for Sema3A expression that guarantees successful intramuscular motor reinnervation by delaying sprouting and reattachment of motoneuron terminals onto damaged muscle fibers early in regeneration pending restoration of muscle fiber contractile integrity.

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Low-pH preparation of skeletal muscle satellite cells can be used to study activation in vitro

Cited by 29 publications

References 20 publications

A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation

A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation

Supplementary immunocytochemistry of hepatocyte growth factor production in activated macrophages early in muscle regeneration

Growth factor regulation of neural chemorepellent Sema3A expression in satellite cell cultures

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