ライフサイエンスコーパス: satellite cell

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

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

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

4 e Drosophila equivalent of vertebrate muscle satellite cells.

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

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

7 eration due to the differentiation defect of satellite cells.

8 and facilitates the generation of postnatal satellite cells.

9 ice intramuscularly injected with engineered satellite cells.

10 differentiation, to maintain PAX7 levels in satellite cells.

11 survival and proliferation of TAK1-deficient satellite cells.

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

13 down in proliferation and differentiation of satellite cells.

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

15 re protein BMAL1 and PER2 in DRG neurons and satellite cells.

16 ive stress and precocious differentiation of satellite cells.

17 scles and sharing properties with vertebrate satellite cells.

18 erformance, and an increase in PAX7 positive satellite cells.

19 the impact of dysfunctional EC signalling on satellite cells.

20 Tw2(+) progenitors are distinct from satellite cells, a muscle progenitor that expresses Pax7

21 atory function, which may contribute to poor satellite cell activation and delayed recovery from musc

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

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

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

25 omoting myogenic regeneration by stimulating satellite cell activation and increasing myofiber fusion

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

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

28 ow that Auf1 transcription is activated with satellite cell activation by stem cell regulatory factor

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

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

31 Satellite cell activation was also observed in burn pati

32 Upon satellite cell activation, p38alpha/beta MAPK phosphoryl

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

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

35 lls but was markedly downregulated following satellite cell activation.

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

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

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

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

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

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

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

43 urther, we demonstrated that EBOV can induce satellite cell and neuronal apoptosis and microglial act

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

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

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

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

48 relatively homogeneous compared to activated satellite cells and committed progenitors, the Hu-MuSC p

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

50 dult EphA7(-/-) mice have reduced numbers of satellite cells and exhibit delayed and protracted muscl

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

52 etween endothelial cells and skeletal muscle satellite cells and is mitogenic for both cell types und

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

54 so studied the effect of Trim33 silencing in satellite cells and the C2C12 mouse muscle cell line.

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

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

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

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

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

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

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

62 Satellite cells are a stem cell population within adult

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

64 Satellite cells are muscle-resident stem cells capable o

65 Muscle satellite cells are myogenic stem cells whose quiescence

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

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

68 Satellite cells are resident adult stem cells that are r

69 Satellite cells are the major myogenic stem cells residi

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

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

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

73 Pax7 expression was unaffected in quiescent satellite cells but was markedly downregulated following

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

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 ls exhibiting characteristics of human fetal satellite cells can be produced in vitro from iPSC, open

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

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

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

81 n of p38 mitogen-activated protein kinase in satellite cells committed to myogenesis.

82 fibre cross-sectional area and the number of satellite cells committed to the myogenic lineage.

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

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

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

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

87 Satellite cell content was reduced in burn patients, wit

88 Satellite cell content, activation and apoptosis were de

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

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

91 ABSTRACT: Satellite cell contribution to unstressed diaphragm is h

92 Similar satellite cell defects have been reported in mouse model

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

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

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

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

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

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

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

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

101 Satellite cell depletion did not alter diaphragm mean fi

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

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

104 Prolonged satellite cell depletion in the diaphragm does not resul

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

106 Whether satellite cell depletion negatively impacts diaphragm qu

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

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

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

110 ayed and protracted muscle regeneration, and satellite cell-derived myogenic cells from EphA7(-/-) mi

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

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

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

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

115 Inhibition of DDR restored satellite cell differentiation ability.

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

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

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

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

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

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

122 lls in developing skeletal muscles and adult satellite cells during homeostasis and muscle regenerati

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

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

125 cise training improves muscle morphology and satellite cell dynamics compared to diet-induced obesity

126 Analysis of satellite cell dynamics on myofibers confirmed that HIF1

127 Satellite cell dysfunction has been shown to underlie th

128 Endothelial and satellite cell dysfunction occur in tandem in many disea

129 muscles and it only slightly enhanced donor satellite cell engraftment in this mouse strain, suggest

130 that is not active in the muscle, and lack a satellite cell equivalent.

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

132 h glucose treated endothelial cells impaired satellite cell expansion and differentiation via decreas

133 Skeletal muscle stem (satellite) cell explants show that Auf1 transcription is

134 ion of similar abnormalities including fewer satellite cells, fewer dividing cells, and an increase i

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

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

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

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

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

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

141 generating muscle from Trim33 knockout mice, satellite cells from Trim33 knockout mice, and C2C12 cel

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

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

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

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

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

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

148 re, MLL1 is required for PAX7 expression and satellite cell function in vivo.

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

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

151 In this process, termed myogenesis, satellite cells get activated, proliferate, and differen

152 Satellite cells grown in CM from HG treated HUVECs reduc

153 reated ECs cause impairments in human muscle satellite cell growth and differentiation in vitro, high

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

155 e on the growth and differentiation of human satellite cells (HMuSC) using a conditioned medium (CM)

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

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

158 criptional regulatory mechanisms controlling satellite cell homeostasis.

159 separate novel subpopulations of human PAX7+ satellite cells (Hu-MuSCs) from normal muscles.

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

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

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

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

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

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

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

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

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

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

170 and differentiation of human skeletal muscle satellite cells in vitro.

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

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

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

174 MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate mu

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

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

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

178 ions and their functional relevance in human satellite cells is lacking.

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

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

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

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

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

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

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

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

187 endothelial cells (ECs) and skeletal muscle satellite cells (MuSC) has been identified as an importa

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

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

190 Satellite cells (muscle stem cells) have been hypothesiz

191 Muscle satellite cells (MuSCs) are the quiescent muscle stem ce

192 ion and their intrinsically deficient muscle satellite cells (MuSCs).

193 tion of embryonic myoblasts and adult muscle satellite cells (MuSCs).

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

195 ed ICAM-1 to be expressed by a population of satellite cells/myoblasts and myofibers.

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

197 myofiber engraftment and ability to seed the satellite cell niche, respond to multiple reinjuries, an

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

199 cells promotes the age-related reduction of satellite cell number and function and contributes to sa

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

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

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

203 bone marrow cells into young animals reduced satellite cell numbers and promoted satellite cells to s

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

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

206 hanced if they were transplanted with either satellite cells, or myofibres, derived from irradiated d

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

208 ly regenerate fibers but provide a quiescent satellite cell pool ensuring long-term maintenance and r

209 eterogeneity is recognized within the murine satellite cell pool, a comprehensive understanding of di

210 y, and premature exhaustion of the quiescent satellite cell pool.

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

212 generation and failed regeneration affecting satellite cell populations.

213 We show that fewer PAX7+ cells occupy a satellite cell position between the myofiber and its ass

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

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

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

217 letion influences muscle fibre regeneration, satellite cell proliferation and differentiation, and in

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 Deletion of Mll1 in satellite cells reduced satellite cell proliferation and self-renewal, and signi

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

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

225 f-function of Rev-erbalpha in vivo augmented satellite cell proliferative expansion and regenerative

226 om irradiated muscle transplanted with donor satellite cells promoted donor cell engraftment in a few

227 Satellite cells provide regenerative capacity to the ske

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

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

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

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

232 elated with fiber hypertrophy (r = 0.49) and satellite cells (r = 0.47).

233 Deletion of Mll1 in satellite cells reduced satellite cell proliferation and

234 Satellite cells remain largely quiescent but are rapidly

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

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

237 al muscle, possibly contributing to the poor satellite cell response observed in older muscle tissue.

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

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

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

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

242 ive muscle disease by irreversibly dampening satellite cell (SC) self-renewal capacity.

243 ependence, and regulation of skeletal muscle satellite cell (SC) subsets remains poorly understood.

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

245 Satellite cells (SC) are muscle stem cells that can rege

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

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

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

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

250 Satellite cells (SCs) are skeletal muscle stem cells tha

251 nctional study of lncRNAs in skeletal muscle satellite cells (SCs) remains at the infancy stage.

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

253 Satellite cells (SCs) reside in a dormant state during t

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

255 Satellite cells (SCs), the resident adult stem cells of

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

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

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

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

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

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

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

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

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

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

266 This satellite cell senescence is due to accumulation of the

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

268 Skeletal muscle satellite cells (SMSCs), the major stem cells responsibl

269 Satellite cell specific knockdown of Tristetraprolin pre

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

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

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

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

274 Mice with satellite-cell-specific Zfp423 deletion exhibit severely

275 ng separation of functionally distinct human satellite cell subpopulations.

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

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

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

279 he recruitment and proliferation of resident satellite cells that exit the cell cycle during the proc

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

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

282 liferation, and differentiation of quiescent satellite cells, the expression of Phospho1 gradually in

283 Satellite cells, the predominant stem cell population in

284 mplicated in increasing myogenic capacity of satellite cells, therefore restoring muscle viability, i

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

286 reduced satellite cell numbers and promoted satellite cells to switch toward a fibrogenic phenotype.

287 Skeletal muscle stem (satellite) cells transplanted into host mouse muscles co

288 Satellite cells undergo concurrent apoptosis and activat

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

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

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

292 The abundance of gammaH2AX+ cells, including satellite cells, was not higher in muscle from old compa

293 Satellite cells were isolated from human skeletal muscle

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

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

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

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

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

299 Transplanted satellite cells with AMPKalpha1 deficiency had severely

300 ain resident stem cells, such as the Pax7(+) satellite cells within skeletal muscle, that regenerate