ライフサイエンスコーパス: satellite cell

1 entiation and fusion of myogenic stem cells (satellite cells).

2 genomic integrity in aged muscle stem cells (satellite cells).

3 enewal and maintenance of muscle stem cells (satellite cells).

4 differentiation, to maintain PAX7 levels in satellite cells.

5 survival and proliferation of TAK1-deficient satellite cells.

6 d for the activation of NF-kappaB and JNK in satellite cells.

7 down in proliferation and differentiation of satellite cells.

8 MPK and induces a Warburg-like glycolysis in satellite cells.

9 ive stress and precocious differentiation of satellite cells.

10 scles and sharing properties with vertebrate satellite cells.

11 on cells and a much larger fraction of their satellite cells.

12 so inhibits differentiation of primary human satellite cells.

13 e Drosophila equivalent of vertebrate muscle satellite cells.

14 to birth, but is not detectable in postnatal satellite cells.

15 , which may compensate for the loss of Pax7+ satellite cells.

16 eration due to the differentiation defect of satellite cells.

17 and facilitates the generation of postnatal satellite cells.

18 ice intramuscularly injected with engineered satellite cells.

19 repair, and regenerate itself by mobilizing satellite cells, a resident population of myogenic proge

20 amts1 as a potent extracellular regulator of satellite cell activation and have significant implicati

21 ng muscle, which was associated with impeded satellite cell activation and impaired muscle regenerati

22 acrophages in vivo is sufficient to increase satellite cell activation and improve muscle regeneratio

23 emonstrating the importance of AMPKalpha1 in satellite cell activation and muscle regeneration.

24 itization of cultured DRG neurons depends on satellite cell activation and on those same NMDAR subuni

25 , macrophages secrete Adamts1, which induces satellite cell activation by modulating Notch1 signaling

26 etabolic activation, an inseparable step for satellite cell activation following muscle injury, have

27 ts that were differentially expressed during satellite cell activation following muscle injury.

28 Satellite cell activation was also observed in burn pati

29 Upon satellite cell activation, p38alpha/beta MAPK phosphoryl

30 Taken together these data show that the satellite cell activation, proliferation, and differenti

31 educes Notch signaling, leading to increased satellite cell activation.

32 ion associated with considerable decrease in satellite-cell activation in p75KO muscle tissue up to 1

33 terstitial fibrogenic cells, which influence satellite cell activity and muscle repair during hypertr

34 ications for understanding the regulation of satellite cell activity and regeneration after muscle in

35 y has led to the hypothesis that the loss of satellite cell activity is also a cause of sarcopenia.

36 le regrowth following a burn injury requires satellite cell activity, underscoring the therapeutic po

37 assign to Ptpn11 signaling a key function in satellite cell activity.

38 The activity of skeletal muscle stem cells, satellite cells, acutely following a severe burn is unkn

39 wing injury occurs through the activation of satellite cells, an injury-sensitive muscle stem cell po

40 isoform expression, cross-sectional area and satellite cell and myonuclear content.

41 ever, the in vivo roles of HIFs in quiescent satellite cells and activated satellite cells (myoblasts

42 rotein beta (C/EBPbeta) is also expressed in satellite cells and acts to maintain the undifferentiate

43 th PDGF-BB showed an increased population of satellite cells and an increase in the number of regener

44 or localised in the extracellular matrix, in satellite cells and close to mitochondria, and involve a

45 spensable for supplementing the reservoir of satellite cells and driving regeneration in normal and d

46 precursors of these adipocytes, we isolated satellite cells and fibro/adipogenic progenitors (FAPs)

47 polarity and directional migration of mouse satellite cells and human myogenic progenitors through a

48 in myotubes, in the extracellular matrix, in satellite cells and in the proximity of mitochondria in

49 s and the cells that contact them, including satellite cells and motor neurons.

50 ted signaling is critical for homeostasis of satellite cells and their function during regenerative m

51 the accumulation of inclusion bodies in the satellite cells and their subsequent degeneration.

52 ithin skeletal myofibers and in trans within satellite cells and within motor neurons via the neuromu

53 muscle differentiation, namely paired box 7 (satellite cell) and early myogenic differentiation and t

54 scription factor in muscle progenitor cells (satellite cells) and myocytes.

55 the dominant AMPKalpha isoform expressed in satellite cells, and AMPKalpha1 deficiency in satellite

56 etween muscle tissue compartments, including satellite cells, and infiltrating myeloid cells upon tis

57 Satellite cells are a stem cell population within adult

58 ctivity and regeneration after muscle injury.Satellite cells are crucial for growth and regeneration

59 Here we report that geriatric satellite cells are incapable of maintaining their norma

60 Satellite cells are muscle-resident stem cells capable o

61 Muscle satellite cells are myogenic stem cells whose quiescence

62 Hh quiescent and that Pax7-expressing muscle satellite cells are not able to give rise to eRMS upon S

63 er, genetic ablation experiments showed that satellite cells are not globally required to maintain my

64 at both proliferation and differentiation of satellite cells are reduced after injury and that muscle

65 Satellite cells are resident adult stem cells that are r

66 Human satellite cells are scarce; therefore, clinical investig

67 Satellite cells are the major myogenic stem cells residi

68 Skeletal muscle stem cells, called satellite cells, are a quiescent heterogeneous populatio

69 vation, proliferation and differentiation of satellite cells, as confirmed in vitro.

70 pe I fibres, with no change in the number of satellite cells associated with MyHC type II fibres.

71 Conditional depletion of satellite cells attenuates recovery of myofibre area and

72 hat IL-6-activated Stat3 signaling regulates satellite cell behavior, promoting myogenic lineage prog

73 known to be essential for the maintenance of satellite cells, but its function in late-stage myogenes

74 cium transients by glutamate or NMDA only in satellite cells, but not in neurons.

75 ntral for regulating the activation state of satellite cells, but the specific extracellular signals

76 CD133+ cells and FKRP L276IKI mouse derived satellite cells by a lentiviral vector expressing the wi

77 ates (muscle proteins, lipids, glucose, DNA (satellite cells)) can be monitored simultaneously and fl

78 s also differentiate into Pax7(+) cells with satellite cell characteristics, including the ability to

79 rofiles of preadipocytes and skeletal muscle satellite cells collected from irradiated mice.

80 SC-Dep mice had >93% depletion of satellite cells compared to SC-WT (P < 0.05).

81 egeneration of damaged muscle fibers and the satellite cell compartment.

82 eover, genetic deletion of myomaker in adult satellite cells completely abolishes muscle regeneration

83 muscle atrophy is associated with decreased satellite cell content and compromised muscle regrowth,

84 ly following a burn, with a net reduction in satellite cell content compared to healthy controls.

85 With the increased satellite cell content following training, an increase i

86 skeletal muscle fibre type distribution and satellite cell content in sedentary subjects.

87 Satellite cell content increased 80% (P < 0.05) 2 days p

88 Satellite cell content was also increased following trai

89 Satellite cell content was reduced in burn patients, wit

90 Satellite cell content, activation and apoptosis were de

91 ned atrophy had decreased muscle progenitor (satellite) cell content.

92 riments that, even in the absence of injury, satellite cells contribute to myofibres in all adult mus

93 ABSTRACT: Satellite cell contribution to unstressed diaphragm is h

94 RNA in myoblast cells and H19 knockout mouse satellite cells decreases differentiation.

95 es from Mtn(-/-)/Errgamma(Tg/+) mouse showed satellite cell deficit which unexpectedly did not affect

96 cells surrounding the SG neurons, leading to satellite cell degeneration and subsequent SG degenerati

97 d, progressing into large vacuoles preceding satellite cell degeneration, and followed by SG degenera

98 ell-specific Pax7(CreER) system in postnatal satellite cells delayed injury-induced muscle repair due

99 uvenile satellite cell-wild-type (SC-WT) and satellite cell-depleted (SC-Dep) mice (8 weeks of age) w

100 x3 mRNA+ cell density in both young and aged satellite cell-depleted diaphragm muscle (P < 0.05), whi

101 Myonuclear density was maintained in young satellite cell-depleted mice regardless of running, alth

102 Following 8 wk of overload, satellite cell-depleted muscle demonstrated an accumulat

103 t and fiber cross-sectional area occurred in satellite cell-depleted muscle.

104 , satellite cell-replete) or tamoxifen (Tam, satellite cell-depleted) treated at 4 months of age and

105 Satellite cell depletion did not alter diaphragm mean fi

106 KEY POINTS: Satellite cell depletion does not affect diaphragm adapt

107 Satellite cell depletion early in life (4 months of age)

108 Prolonged satellite cell depletion in the diaphragm does not resul

109 Up-regulation of Pax3 mRNA+ cells after satellite cell depletion in young and aged mice suggests

110 Whether satellite cell depletion negatively impacts diaphragm qu

111 stant by preventing myonuclear accretion via satellite cell depletion, both the number of transcripti

112 vo diaphragm function was also unaffected by satellite cell depletion.

113 ent with this, the in vitro proliferation of satellite cells derived from these muscles was reduced b

114 Satellite cell-derived myoblasts lacking MEF2A, C, and D

115 Here we have used human primary CD56(Pos) satellite cell-derived myogenic progenitors obtained fro

116 the cells adhere, the effect of elastase on satellite cell-derived primary myoblast growth and diffe

117 Bhlhe40 is strongly induced by hypoxia in satellite cell-derived primary myoblasts.

118 elerated nor exacerbated sarcopenia and that satellite cells did not contribute to the maintenance of

119 o/adipogenic progenitors (FAPs) from muscle; satellite cells did not differentiate into adipocytes ev

120 Inhibition of DDR restored satellite cell differentiation ability.

121 ormed AT2R promoter reporter analysis during satellite cell differentiation and found that the 70 bp

122 al and redundant roles of MEF2A, C, and D in satellite cell differentiation and identify a MEF2-depen

123 an ischemic hypoxia environment that impedes satellite cell differentiation and reduces the efficienc

124 le regeneration, implicating MUNC in primary satellite cell differentiation in the animal.

125 nt degradation of EZH2 is a prerequisite for satellite cells differentiation and identify PJA1 as a n

126 response in muscle stem cells (also known as satellite cells) differs between aged and young mice.

127 muscle function but a >70% loss of Rbfox1 in satellite cells does not disrupt muscle regeneration.

128 iption factors induce myomaker expression in satellite cells during acute and chronic muscle regenera

129 eatures and biological functions of Pax7(Lo) satellite cells during muscle development and regenerati

130 To determine the necessity of satellite cells during muscle recovery following a burn

131 Analysis of satellite cell dynamics on myofibers confirmed that HIF1

132 Satellite cell dysfunction has been shown to underlie th

133 MyoD genes drives the de novo myogenesis in satellite cells even in aged muscle.

134 Moreover, TAK1-deficient satellite cells exhibit increased oxidative stress and u

135 ontrast, transient Stat3 inhibition promoted satellite cell expansion and enhanced tissue repair in b

136 oncurrent activation and apoptosis of muscle satellite cells following a burn injury in paediatric pa

137 ation mainly causes ERMS that originate from satellite cells following a process of multistep progres

138 rent study was to determine the necessity of satellite cells for long-term muscle growth and maintena

139 rval newts use stem/progenitor cells such as satellite cells for new muscle in a regenerated limb, wh

140 ction of active chromatin marks in activated satellite cells from aged mice, resulting in the specifi

141 ered epigenetic stress response in activated satellite cells from aged mice, which limits satellite c

142 itogen-activated protein kinase signaling in satellite cells from aged mice.

143 cessary and sufficient for the transition of satellite cells from G0 into G(Alert) and that signallin

144 ferentiation on C2C12 myoblasts, and primary satellite cells from mouse and human, we show that culli

145 of Hoxa9 mimics ageing-associated defects in satellite cells from young mice, which can be rescued by

146 satellite cells from aged mice, which limits satellite cell function and muscle regeneration by Hoxa9

147 tin activation or deletion of Hoxa9 improves satellite cell function and muscle regeneration in aged

148 However, signalling mechanisms that regulate satellite cell function are less understood.

149 entification of signaling pathways affecting satellite cell function during aging may provide insight

150 markers would be powerful tools for studying satellite cell function during homeostasis and in pathog

151 de most of the currently known inhibitors of satellite cell function in ageing muscle, including Wnt,

152 a well-defined transcriptional regulator of satellite cell functions that defines two subpopulations

153 pendent of donor age, as few as 2 to 4 PAX7+ satellite cells gave rise to several thousand myoblasts.

154 represents a decisive factor that separates satellite cell gene expression in aged mice from that in

155 ific stem cells and suggest that these PAX7+ satellite cells have potential to restore gene function

156 y expressed in the skeletal muscle, mediates satellite cell heterogeneity by fine-tuning Pax7 levels

157 Our insights into a critical mechanism in satellite cell homeostasis during muscle regeneration co

158 PR plays a pivotal role in the regulation of satellite cell homeostasis during regenerative myogenesi

159 criptional regulatory mechanisms controlling satellite cell homeostasis.

160 ighlight an age-associated deregulation of a satellite cell homeostatic network and reveal potential

161 Depletion of satellite cells impaired post-burn recovery of both musc

162 own about the molecular effectors underlying satellite cell impairment and depletion.

163 atellite cells, and AMPKalpha1 deficiency in satellite cells impairs their activation and myogenic di

164 ts play a critical role in the regulation of satellite cells in adult and aged skeletal muscle.

165 tenance, we genetically labelled and ablated satellite cells in adult sedentary mice.

166 Additionally, a significant percentage of satellite cells in burn patients expressed Ki67, a marke

167 d d genes, singly and in combination, within satellite cells in mice, using tamoxifen-inducible Cre r

168 g evidence for a fibre type-specific role of satellite cells in muscle adaptation following aerobic t

169 d to counteract the functional exhaustion of satellite cells in pathological conditions, thereby main

170 that allows for the conditional depletion of satellite cells in skeletal muscle.

171 These findings support an integral role for satellite cells in the aetiology of lean tissue recovery

172 x3+ cells may compensate for a loss of Pax7+ satellite cells in the diaphragm.

173 y, underscoring the therapeutic potential of satellite cells in the prevention of prolonged frailty i

174 of glial fibrillary acidic protein by glial satellite cells in the trigeminal ganglia, the location

175 Skeletal muscle satellite cells in their niche are quiescent and upon mu

176 rvival and differentiation of PERK-deficient satellite cells in vitro and muscle formation in vivo.

177 wn of Tristetraprolin precociously activates satellite cells in vivo, enabling MyoD accumulation, dif

178 e sedentary mice by experimentally depleting satellite cells in young adult animals to a degree suffi

179 ctivity in the presence and absence of Pax7+ satellite cells in young and aged mice using an inducibl

180 peractivity in activated, but not quiescent, satellite cells induces ERMS with high penetrance and sh

181 Inactivation of TAK1 in satellite cells inhibits muscle regeneration in adult mi

182 of PERK, but not the IRE1 arm of the UPR in satellite cells inhibits myofiber regeneration in adult

183 he survival and differentiation of activated satellite cells into the myogenic lineage.

184 The absence of MEF2A, C, and D in satellite cells is associated with aberrant expression o

185 ed activation of muscle stem cells (known as satellite cells) is critical for postnatal muscle growth

186 n unclear, the skeletal muscle stem cell, or satellite cell, is required for muscle regeneration.

187 edifferentiates myocytes into Pax7 quiescent satellite cells, leading to severe defects in muscle gro

188 ibers that enabled development of quiescent, satellite cell-like progenitors and a model for Duchenne

189 In geriatric mice, resting satellite cells lose reversible quiescence by switching

190 egulatory factors, while down-regulating the satellite cell marker Pax7.

191 Satellite cell markers did not correlate with Ki-67-affe

192 of replicative senescence, decline in muscle satellite cell-mediated regeneration coincides with acti

193 d contribute to FSHD pathology by preventing satellite cell-mediated repair.

194 pigenetic regulator that connects changes in satellite cell metabolism with changes in the transcript

195 vitro, suggesting a novel role for activated satellite cells/MPCs in muscle adaptation.

196 d topographies differentiate cells towards a satellite cell muscle progenitor state - a distinct cell

197 were localised in the extracellular matrix, satellite cells (muscle stem cells) and close to mitocho

198 Satellite cells (muscle stem cells) have been hypothesiz

199 s in quiescent satellite cells and activated satellite cells (myoblasts) are poorly understood.

200 e results suggest that lifelong reduction of satellite cells neither accelerated nor exacerbated sarc

201 al biomimetic muscle tissues with a resident satellite cell niche and capacity for robust myogenesis

202 We found that short-term CR increased the satellite cell number and collagen VI content of muscle,

203 rrelated with treatment-induced increases in satellite cell number and several muscle-specific abnorm

204 Focal adhesion kinase activation and satellite cell number are elevated in muscles undergoing

205 distribution, muscle atrophy, an increase in satellite cell number, and a decrease in activity of cre

206 e muscle phenotype positively correlate with Satellite cell number, the resident stem cells of skelet

207 ter cardiotoxin injury, as well as increased satellite cell numbers and activity.

208 regenerative capacity of a muscle even when satellite cell numbers are reduced.

209 Selective deletion of Traf6 in satellite cells of adult mice led to profound muscle reg

210 entary (-7%) and running (-19%) mice without satellite cells (P < 0.05).

211 ice with gene disruption in muscle precursor/satellite cells (Pax7-Cre/cKO), uncoupling of AChRs from

212 Skeletal muscle-derived stem cells, called satellite cells, play essential roles in regeneration af

213 scle tissue, and self-renew to replenish the satellite cell population.

214 ion of resistance to oxidative stress in the satellite cell population.

215 in burn patients, with approximately 20% of satellite cells positive for TUNEL staining, indicating

216 tors (myoblasts) that become Pax7(+) MyoD(-) satellite cells prior to birth, but is not detectable in

217 The activation and apoptosis of satellite cells probably impacts the recovery of lean ti

218 Severe burn injury induces satellite cell proliferation and fusion into myofibres w

219 injury induced skeletal muscle regeneration, satellite cell proliferation and fusion.

220 TAK1 is essential for satellite cell proliferation and its inactivation causes

221 ng muscle regeneration through activation of satellite cell proliferation and migration.

222 ated levels of TWEAK, which stimulate muscle satellite cell proliferation and tissue regeneration in

223 vided 5-ethynyl-2'-deoxyuridine to determine satellite cell proliferation, activation and fusion.

224 Ablation of TRAF6 also increases satellite cells proliferation and myofiber regeneration

225 Muscle satellite cells promote regeneration and could potential

226 Previous studies showed porcine muscle satellite cells (PSCs) are important for postnatal skele

227 We show that modulating satellite cell quiescence via intramuscular injection of

228 stand the mechanisms involved in maintaining satellite cell quiescence, we identified gene transcript

229 ignaling is antagonized by SPRY1 to maintain satellite cell quiescence.

230 effect of Wnt signaling on the activation of satellite cells, rather than Wnt-mediated fibrosis, was

231 Satellite cell regenerative functions decline with agein

232 These results provide evidence that satellite cells regulate the muscle environment during g

233 Satellite cells remain largely quiescent but are rapidly

234 Mice were vehicle (Veh, satellite cell-replete) or tamoxifen (Tam, satellite cel

235 rauma and we propose that an impaired muscle satellite cell response is key in the aetiology of burn-

236 p16(INK4a) silencing in geriatric satellite cells restores quiescence and muscle regenerat

237 itional ablation of Stat3 in Pax7-expressing satellite cells resulted in their increased expansion du

238 ate muscle differentiation, homeostasis, and satellite cell (SC) activation.

239 isease's pathological changes, the degree of satellite cell (SC) dysfunction defines disease progress

240 mation, fibrosis, mitochondrial dysfunction, satellite cell (SC) exhaustion and loss of skeletal and

241 Here we investigate the relevance of the satellite cell (SC) niche in sarcoma development by usin

242 protein breakdown and apoptosis and inhibits satellite cell (SC) proliferation and muscle regeneratio

243 for the skeletal muscle stem cell, i.e., the satellite cell (SC), is incomplete.

244 Primary quiescent satellite cells (SC) from chow-fed DKO mice, not in Ldlr

245 le mouse KO that specifically ablates Utx in satellite cells (SCs) and demonstrated that active H3K27

246 Satellite cells (SCs) are adult muscle stem cells that a

247 Satellite cells (SCs) are myogenic stem cells required f

248 While satellite cells (SCs) have long been recognized as the m

249 muscle health; however, its effect on muscle satellite cells (SCs) remains largely unknown.

250 onse after muscle injury, focusing on muscle satellite cells (SCs), inflammatory reaction, fibrosis,

251 Using muscle stem cells, or satellite cells (SCs), we found that autophagy, which ca

252 endent on the resident stem cell population, satellite cells (SCs).

253 is associated with functional impairment of satellite cells (SCs).

254 due to deficiencies in resident stem cells (satellite cells, SCs) and derived myogenic progenitors (

255 matic hyperplasia of muscle stem cells (i.e. satellite cells, SCs) but surprisingly without affecting

256 and maintenance; however muscle stem cells (satellite cells, SCs), are deemed to have little impact

257 ifferentiation of LRCs in vitro and impaired satellite cell self-renewal after muscle injury.

258 and regeneration in aged muscles, decreased satellite cell self-renewal and regenerative potential,

259 er normoxia but are required for maintaining satellite cell self-renewal in hypoxic environments.

260 ulated by Notch signaling, a key governor of satellite cell self-renewal.

261 ion of Notch signaling, a key determinant of satellite cell self-renewal.

262 e to impaired muscle growth, associated with satellite cell senescence and premature sarcopenia.

263 This satellite cell senescence is due to accumulation of the

264 Activity of satellite cells, skeletal muscle stem cells, is altered

265 Satellite cell specific knockdown of Tristetraprolin pre

266 tellite cells, which is abolished because of satellite cell-specific AMPKalpha1 knock-out.

267 prove muscle regeneration in obese mice with satellite cell-specific AMPKalpha1 knockout, demonstrati

268 We also determined that satellite cell-specific deletion of Traf6 exaggerates th

269 ducible Cre recombinase under control of the satellite cell-specific Pax7 promoter.

270 a dKO produced with the tamoxifen-inducible, satellite cell-specific Pax7(CreER) system in postnatal

271 els, inclusion body accumulation was seen in satellite cells surrounding spiral ganglion (SG) neurons

272 ads to progressive sulfatide accumulation in satellite cells surrounding the SG neurons, leading to s

273 ap1CKO mouse skeletal muscle contained fewer satellite cells than normal and these cells had evidence

274 depends on a population of adult stem cells (satellite cells) that remain quiescent throughout life.

275 ted muscle stem cells (MuSCs), also known as satellite cells, that reside in anatomically defined nic

276 y, we identify skeletal muscle stem cell, or satellite cells, that retain (LRC) or lose (nonLRC) the

277 Strikingly, however, satellite cells, the adult muscle stem cells that are es

278 from a decline in the number and function of satellite cells, the direct cellular contributors to mus

279 Satellite cells, the predominant stem cell population in

280 16(INK4a) is dysregulated in human geriatric satellite cells, these findings provide the basis for st

281 ich modulate Notch signaling in the adjacent satellite cells to enhance their regenerative capacity.

282 skeletal muscle involves fusion of activated satellite cells to form new myofibers.

283 ver, loss of CryAB altered the capability of satellite cells to regenerate skeletal muscle.

284 se, which is a low stress exercise, converts satellite cells to the activated state due to accelerate

285 generation, and proper homing of human PAX7+ satellite cells to the stem cell niche.

286 extensively investigated, the regulation of satellite cells under steady state during the adult stag

287 Satellite cells undergo concurrent apoptosis and activat

288 hat levels of PERK and IRE1 are increased in satellite cells upon muscle injury.

289 ed and oncogenic Kras is activated in muscle satellite cells via a Pax7(CreER) driver following intra

290 sites of muscle injury induce activation of satellite cells via expression of Adamts1.

291 use models specific to muscle stem cells (or satellite cells), we show that mTORC1 activity is necess

292 PAX7+ satellite cells were activated and proliferated efficien

293 during aging between the loss of activity of satellite cells, which are endogenous muscle stem cells,

294 ng noncanonical Shh promote proliferation of satellite cells, which is abolished because of satellite

295 al Shh pathway to Warburg-like glycolysis in satellite cells, which is required for satellite activat

296 Juvenile satellite cell-wild-type (SC-WT) and satellite cell-depl

297 In adult muscle, quiescent satellite cells will transition into an active state in

298 Transplanted satellite cells with AMPKalpha1 deficiency had severely

299 ered gene expression in cultured human PAX7+ satellite cells with Sleeping Beauty transposon-mediated

300 ng for the conditional depletion of > 90% of satellite cells with tamoxifen treatment.