ライフサイエンスコーパス: myofiber

1 the even positioning of nuclei in the mature myofiber.

2 d necrotic region and increased regenerating myofibers.

3 f dystrophin expression in the sarcolemma of myofibers.

4 robustness of the response to denervation of myofibers.

5 the rate of elimination on fast versus slow myofibers.

6 ring calcium sensitivity or cooperativity of myofibers.

7 fuses specifically to type IIb/x fast-twitch myofibers.

8 tivity to facilitate hypertrophy of type IIb myofibers.

9 nflammation or adipogenic replacement of the myofibers.

10 associated with loss of type 2b fast-twitch myofibers.

11 edominantly contained in fast twitch/type II myofibers.

12 flammation and adipogenic replacement of the myofibers.

13 usion of PMO-loaded myoblasts into repairing myofibers.

14 tivated mainly in muscle progenitors and not myofibers.

15 nment of scaffold nanofibers with endogenous myofibers.

16 h fusion of myoblasts to form multinucleated myofibers.

17 tes fusion of exogenous myoblasts to injured myofibers.

18 nonucleated myoblasts to form multinucleated myofibers.

19 e to form multi-layered bundles with aligned myofibers.

20 most enriched in exosomes compared to parent myofibers.

21 he extracellular matrix (ECM) that surrounds myofibers.

22 uch-evoked motility, and highly disorganized myofibers.

23 yofibers fail to grow at the same rate as WT myofibers.

24 n of myoblasts preferentially at the tips of myofibers.

25 pment, myoblasts fuse to form multinucleated myofibers.

26 ith dystrophin at the sarcolemma in skeletal myofibers.

27 ouse by blunting the regeneration of injured myofibers.

28 er of embryonic myosin-positive regenerating myofibers.

29 in the size of MHC IIA positive or high SDH myofibers.

30 functional cytoplasmic volumes in developing myofibers.

31 population of satellite cells/myoblasts and myofibers.

32 nal diversity within multinucleated skeletal myofibers.

33 n in mice in which signaling was targeted in myofibers.

34 se in immunoreactivity surrounding atrophied myofibers.

35 process of myogenic differentiation to form myofibers.

36 ivity inhibits MP fusion and contribution to myofibers.

37 d in cardiac myocytes and oxidative skeletal myofibers.

38 bodies/exosomes marker CD63 in regenerating myofibers.

39 transferases, as a gene enriched in type IIb myofibers.

40 to be sequentially executed in living single myofibers.

41 s seeding-competent amyloid that is toxic to myofibers.

42 ssed by type I and IIa myofibers but not IIb myofibers.

43 Nos1, and structural genes, such as Myl1, in myofibers.

44 erativity, or calcium-ATPase activity in the myofibers.

45 localized at the sarcolemma of regenerating myofibers.

46 rors were, respectively, 0.179 +/- 0.050 for myofiber, 0.049 +/- 0.017 for cross-fiber, and 0.039 +/-

47 hnology for use on whole-mount mouse primary myofibers, a preparation that isolates single myofibers

48 bedded within the fibrotic areas between the myofibers adjacent to the collagen type I fibers.

49 hesis, and the organization of nuclei within myofibers after myogenic cell fusion.

50 or imaging revealed reduced reorientation of myofiber aggregates during cardiac contraction in patien

51 a more longitudinal orientation of diastolic myofiber aggregates was measured compared with controls.

52 ate myocytes upon muscle damage, forming new myofibers along with self-renewing stem cells in prepara

53 Targeting signaling specifically in myofibers also led to reductions in overall body fat con

54 Single myofiber analysis of fast-contracting extensor digitorum

55 To address this question, a conditional Ctgf myofiber and fibroblast-knockout mouse lines were genera

56 occupy a satellite cell position between the myofiber and its associated basal lamina in Six1 and Six

57 matically affects calcium sensitivity of the myofiber and systolic and diastolic functions.

58 we applied laser wounding to live mammalian myofibers and assessed translocation of fluorescently ta

59 of functional dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle bioc

60 t transcript levels in mdx muscles, isolated myofibers and DMD immortalized myoblasts.

61 results in regenerating muscles with smaller myofibers and fat accumulation.

62 ng-related phenotypes in cis within skeletal myofibers and in trans within satellite cells and within

63 ged mice and results from 15-PGDH-expressing myofibers and interstitial cells, such as macrophages, w

64 we investigated skeletal muscle pathology in myofibers and myofibrils isolated from young hetero- and

65 eneration and regeneration of multinucleated myofibers and pathological activation of a variety of ot

66 enerated a new conditional knockout of MR in myofibers and quantified cell-intrinsic mechanistic effe

67 X7(+) cells generated in culture can produce myofibers and self-renew in vitro and in vivo Together,

68 ing, involves coordinate changes in skeletal myofibers and the cells that contact them, including sat

69 eins across the length and depth of skeletal myofibers and their associated stem cells.

70 gnized myonuclear subtypes within dystrophic myofibers and uncover degenerative and regenerative tran

71 rogenitor stage to terminally differentiated myofibers, and discuss how this knowledge has been appli

72 sarcolemmal disruption compared to Dysf(129) myofibers, and impaired translocation of annexin A6 asso

73 scle inflammation, adipogenic replacement of myofibers, and improved muscle function.

74 Our results show that the myofibers are critical mediators of the deleterious effe

75 nalyze the whole transcriptome of individual myofibers are lacking.

76 Skeletal muscle myofibers are large syncytial cells comprising hundreds

77 possess fewer myofibers at birth, and those myofibers are reduced in size and have fewer myonuclei a

78 icant increases in muscle mass, showing that myofibers are the direct target for signaling by these l

79 Muscle mass and myofiber area were decreased 20-30% in STZ-Diabetes mice

80 controls, which correlated with decreases in myofiber area, limb strength, and treadmill time/distanc

81 ts that depict the macroscale orientation of myofiber arrays.

82 al dyW-/- muscles display the same number of myofibers as wildtype (WT) muscles, but by E18.5 dyW-/-

83 A7(-/-) mice, hindlimb muscles possess fewer myofibers at birth, and those myofibers are reduced in s

84 ove the membrane integrity of the dystrophic myofibers at the time of AAV-U7 injection, mdx muscles w

85 also led to impaired muscle force and caused myofiber atrophy and degeneration.

86 lcoholic myopathy, which is characterized by myofiber atrophy and the loss of muscle strength.

87 loss of skeletal muscle mass associated with myofiber atrophy or alter a variety of in situ and ex vi

88 in size and contractile speed, with type IIb myofiber being the largest and fastest.

89 diponectin accumulated on plasma membrane of myofibers both in mice and human, and intracellularly co

90 rough mechanisms involving the regulation of myofiber branching, protein synthesis, and the organizat

91 (p < 0.001) and matured into 0.5 mm diameter myofiber bundles with greater 3D cell alignment and high

92 and for Nrp1, is expressed by type I and IIa myofibers but not IIb myofibers.

93 laminin alpha2 surrogates in mature skeletal myofibers, but it increased the number of embryonic myos

94 nalyze the whole transcriptome of individual myofibers by combining single-fiber isolation with Switc

95 rophin-null phenotype were increased ectopic myofiber calcification and altered macrophage infiltrati

96 ure postnatal deletion of Pofut1 in skeletal myofibers can induce aging-related phenotypes in cis wit

97 ng DNA and restored the Dmd reading frame in myofibers, cardiomyocytes, and muscle stem cells after l

98 enhancers specify muscles in accordance with myofiber composition, show little resemblance to culture

99 Analysis of satellite cell dynamics on myofibers confirmed that HIF1alpha/2alpha dKO myoblasts

100 I examined the influence of target myofiber contractile properties on synapse elimination.

101 s a hitherto unknown function independent of myofiber contraction.

102 no alterations in calcium sensitivity of the myofibers, cooperativity, or calcium-ATPase activity in

103 pericyte transplantation recovered losses in myofiber cross-sectional area and the capillary-to-fiber

104 DNF treatment, few changes were seen in mean myofiber cross-sectional areas compared to age-matched n

105 als (24.6 mum(2)/kg; IQR, 21.6-26.0), median myofiber cross-sectional areas normalized to weight and

106 The decreased myofiber damage translated into a significant increase i

107 ch stabilizes the sarcolemma leading to less myofiber degeneration and increased regeneration.

108 ) was accomplished and histopathology showed myofiber degeneration in 3 HERDA horses and 1 control.

109 e surrounding the plane of dissection showed myofiber degeneration, fat deposition, and reduction of

110 zation studies in human muscle and zebrafish myofibers demonstrate that PYROXD1 localizes to the nucl

111 High-resolution imaging of live myofibers demonstrated that fibers from Dysf(B6) mice di

112 Treatment of NIH 3T3 cells with myofiber-derived exosomes downregulated the miR-133a tar

113 uced expression of miRs 1, 133a, and 133b in myofiber-derived exosomes.

114 ficantly decreased muscle atrophy, increased myofiber diameter, and improved SFI.

115 and grow normally to adulthood with smaller myofiber diameter, diminished physical performance, and

116 ofibers, reduced variance, increased size of myofiber diameters, reduced myofiber immunoglobulin G up

117 scriptional return on a per nuclear basis in myofibers diminishes, which accounts for both the absolu

118 Cases with typical features but no myofiber disarray were considered possible HCM.

119 The typical increase in myofiber DNA content observed at the later stage of hype

120 stently associated with the formation of new myofibers during embryonic development, postlarval growt

121 promotes nutrient uptake and catabolism into myofibers during exercise in an osteocalcin-dependent ma

122 mbryonic and fetal myogenesis and on nascent myofibers during muscle regeneration in vivo.

123 t in a pathway that affects the alignment of myofibers during the development of the ventricular sept

124 following transplantation they show superior myofiber engraftment and ability to seed the satellite c

125 eus muscle in mice genetically deficient for myofiber ERK1/2.

126 ion, we find that individual nuclei within a myofiber establish different local scaling relationships

127 Furthermore, stac3(NAM) myofibers exhibited increased caffeine-induced Ca(2+) re

128 Isolated myofibers expressing lacZ were imaged with and without a

129 These results suggest that fetal dyW-/- myofibers fail to grow at the same rate as WT myofibers.

130 Inner pectinate myofibers form mainly by direct branching, unlike delami

131 -Myomaker pair controls the critical step in myofiber formation during muscle development.

132 al muscle construct shows the improvement of myofiber formation, long-term survival, and neuromuscula

133 which is composed of numerous multinucleated myofibers formed by the fusion of progenitor cells durin

134 aggregates, improves muscle force, protects myofibers from the pathology-derived turnover and decrea

135 yzed the differences in the transcriptome of myofibers from young and old mice to validate the effect

136 that Pit1 and Pit2 are essential for normal myofiber function and survival, insights which may impro

137 ing satellite cell activation and increasing myofiber fusion.

138 muscle-targeted Lrrc8a KO mice have smaller myofibers, generate less force ex vivo, and exhibit redu

139 te muscle repair, yet the ability to enhance myofiber growth following disuse is unknown.

140 enerate enough muscle cells to sustain fetal myofiber growth.

141 equirement to achieve efficient hypertrophic myofiber growth.

142 ts for both the absolute reliance developing myofibers have on nuclear accrual to establish size, and

143 reathing rate 2 SMS excitation in transmural myofiber helix angle, mean diffusivity (mean +/- standar

144 Myofiber helix angle, mean diffusivity, fractional aniso

145 d histological assays are available to study myofiber heterogeneity, efficient methods to analyze the

146 (+/+)) at eight months of age as a result of myofiber hyperplasia.

147 Thus, inhibition of myofiber hypertrophic growth is a consistent feature of

148 Inhibition of Chronos induces myofiber hypertrophy both in vitro and in vivo, in part,

149 skeletal muscle growth and overload-induced myofiber hypertrophy in mice.

150 h stimulus is sufficient to ensure long-term myofiber hypertrophy.

151 Fc could improve weakness in NM mice through myofiber hypertrophy.

152 ncreased size of myofiber diameters, reduced myofiber immunoglobulin G uptake, and reduced muscle was

153 le strip composed of differentiated skeletal myofibers in a matrix of natural proteins, including fib

154 ther alone or in combination specifically in myofibers in mice.

155 tion and metabolic programming of glycolytic myofibers in skeletal muscle.

156 as a loss of Abl2 leads to excessively long myofibers in the diaphragm, intercostal and levator auri

157 nesis and restricted to mature type I (slow) myofibers in the muscle.

158 Myofibers in the ventricular septum follow a stereotypic

159 The formation of new myofibers in vertebrates occurs by myoblast fusion and r

160 Myofibers increase size and DNA content in response to a

161 nds of these muscle islands, suggesting that myofibers induce differentiation of tendon cells, which

162 Depleting its synthesis in skeletal myofibers induces vacuolization and contraction impairme

163 and is required for postnatal maintenance of myofiber innervation by motor neurons.

164 he DMD gene, encoding dystrophin, compromise myofiber integrity and drive muscle deterioration in Duc

165 with either of these genes severely disrupts myofiber integrity and dystrophin localization, suggesti

166 that they may function similarly to maintain myofiber integrity.

167 to dystrophic skeletal muscles through both myofiber intrinsic effects on muscle force and downstrea

168 Resealing of tears in the sarcolemma of myofibers is a necessary step in the repair of muscle ti

169 due to fibrotic or adipogenic replacement of myofibers is common in muscle diseases and muscle-reside

170 ever, the mechanism by which it functions in myofibers is not clear.

171 We show that targeting signaling in myofibers is sufficient to cause significant increases i

172 of tendon cells, which reciprocally regulate myofiber length and orientation.

173 Increased myofiber length is caused by enhanced myoblast prolifera

174 kinase 2 (Abl2) has a key role in regulating myofiber length, as a loss of Abl2 leads to excessively

175 Despite massive hypertrophy on the myofiber level, we report no hypertrophy on the muscle l

176 are explained by previously underappreciated myofiber loss in mdx mice.

177 or necrotic cell death during stages of peak myofiber loss, countering well-supported assumptions of

178 We conclude that due to myofiber loss, in combination with the progressive natur

179 ion did not scale with cell size, as smaller myofibers (<1000 mum(2)) demonstrated the highest transc

180 ediate, cell-intrinsic mechanisms as well as myofiber/macrophage interactions.

181 ve accumulation of Annexin A2 (AnxA2) in the myofiber matrix causes FAP differentiation into adipocyt

182 ized complex is essential for muscle growth, myofiber maturation, and muscle cell survival and that a

183 rent nuclei within the shared cytoplasm of a myofiber may display transcriptional diversity and wheth

184 data suggest that VEGF expressed by skeletal myofibers may directly or indirectly regulate both hippo

185 roblasts, whereas ezrin colocalized with the myofiber membranes.

186 robably due to alterations of the dystrophic myofiber membranes.

187 er individual nuclei within a multinucleated myofiber might respond differentially to DMD pathogenesi

188 was ~80% reduced, fibrosis was reduced, and myofiber morphology normalized.

189 mbrane integrity after injury independent of myofiber MR.

190 lates strongly with their proportion of slow myofibers: muscles with more slow fibers undergo elimina

191 letal muscle to produce movement, individual myofibers must form stable contacts with tendon cells an

192 repair/integrity leads to calcium influx and myofiber necrosis leading to progressive dystrophic dise

193 membrane ruptures and leakiness that induces myofiber necrosis, a subsequent inflammatory response, a

194 ic mice overexpressing Ctss showed increased myofiber necrosis, muscle histopathology, and a function

195 These mutant mice displayed myofiber necrosis, weaker muscle strength, reduced locom

196 Subendocardial myofibers normally run in parallel along the left ventri

197 ally, terminally differentiated, postmitotic myofiber nuclei from obese individuals had elevated gamm

198 ormalities and heterogeneity associated with myofiber nuclei, as well as other mononucleated cell typ

199 sferrin-mediated iron uptake by regenerating myofibers occurs independently of systemic iron homeosta

200 gineered muscle fibers that mimic the native myofiber of the MuSC niche.

201 pregulated in the undamaged and regenerating myofibers of injured muscles.

202 This interaction is present in regenerating myofibers of patients with Duchenne muscular dystrophy,

203 n of the intermediate filament desmin in the myofibers of the patients.

204 Ectopic muscle islands, each composed of myofibers of uniform length and orientation, form within

205 evealed their increased expression in mature myofibers of WB-affected chickens.

206 We performed a thorough characterization of myofiber pathology in mdx mice from 2 weeks to 2 years o

207 is study also confirms the existence of slow myofiber-phenotype and provides mechanistic insights int

208 ies have hypothesized the occurrence of slow myofiber-phenotype, and dysregulation of lipid metabolis

209 d with mutations in genes that stabilize the myofiber plasma membrane, such as through the dystrophin

210 hypothesized that VEGF produced by skeletal myofibers plays a role in regulating hippocampal neurona

211 of genes encoding normal cardiac slow-twitch myofiber proteins and pathologically increased expressio

212 ssion of genes encoding skeletal fast-twitch myofiber proteins.

213 scripts are uniformly distributed throughout myofibers, proximity to specialized regions can affect t

214 Pofut1 deletion in skeletal myofibers reduced NotchR signaling in young adult muscle

215 showed reduced levels of centrally nucleated myofibers, reduced variance, increased size of myofiber

216 Blocking FAP ciliation also enhanced myofiber regeneration after injury and reduced myofiber

217 eased membrane leakiness and damage owing to myofiber regeneration and enhanced support at the extrac

218 ating muscle-specific gene expression during myofiber regeneration and have revealed a physiological

219 ng PMO administration coincide with areas of myofiber regeneration and inflammation.

220 s to decreased muscle fibrosis and increased myofiber regeneration following IR injury, suggesting sh

221 ately mitigated muscle fibrosis and improved myofiber regeneration following IR injury.

222 1 arm of the UPR in satellite cells inhibits myofiber regeneration in adult mice.

223 Loss of UTX in SCs blocked myofiber regeneration in both male and female mice.

224 within adult muscle and are responsible for myofiber regeneration upon injury.

225 estoration occurs preferentially in areas of myofiber regeneration, where antisense oligonucleotides

226 In this study, we found that cultured myofibers release nanovesicles that have bilamellar memb

227 is not known whether skeletal muscle fibers (myofibers) release exosomes.

228 k of annexin A2 (AnxA2) also results in poor myofiber repair and progressive muscle weakening with ag

229 of AnxA2-deficient muscle we find that poor myofiber repair due to the lack of AnxA2 does not result

230 n muscle repair, which includes facilitating myofiber repair, chronic muscle inflammation and adipoge

231 ression of annexins A1 and A6, which mediate myofiber repair.

232 h as trophoblasts, osteoclasts, and skeletal myofibers require multinucleation.

233 Here, we report on a single-myofiber RNA-sequencing (smfRNA-Seq) approach to analyze

234 n the mdx background significantly increased myofiber sarcolemmal membrane stability with greater exp

235 Only myofiber-selective inhibition of CTGF protected delta-sa

236 alphaLNNd also restored myofiber shape, size, and numbers to control levels in d

237 n myotube cultures was sufficient to promote myofiber shrinkage, consistent with enhanced protein cat

238 e, P < 0.0001, N = 5-10/group) and decreased myofiber size (1661 +/- 134 mum(2) vs. 2221 +/- 100 mum(

239 ofiber regeneration after injury and reduced myofiber size decline in the muscular dystrophy model.

240 , may be responsible for shift of Hmox1(-/-) myofiber size distribution toward larger one.

241 eosinophil infiltration in association with myofiber size distribution, centralized nuclei, serum cr

242 Ablation of MyD88 reduces myofiber size during muscle regeneration, whereas its ov

243 g finger protein 1 (MuRF1) up-regulation and myofiber size reduction.

244 onstrate that Mettl21e functions to maintain myofiber size through inhibiting proteasome-mediated pro

245 Although a reduction in myofiber size was apparent, EDL and SOL myonuclear numbe

246 egenerating myofibers were more abundant and myofiber size was larger for wild-type compared with Ica

247 reases in body mass, muscle mass, quadriceps myofiber size, and survival, but other measurements of s

248 skeletal muscle size and strength, decreased myofiber size, increased slow fiber (type 1) density, in

249 muscle differentiation in vitro and skeletal myofiber size, muscle function, adiposity and systemic m

250 in the expression of genes known to regulate myofiber size.

251 Nr4a3) had minimal effect on muscle mass and myofiber size.

252 y in Nur77 exhibited reduced muscle mass and myofiber size.

253 Myofiber smallness is also found in many cases of NM and

254 n was demonstrated in vivo in mice harboring myofiber-specific deletion of VEGF-A (mVEGF(-/-)) and in

255 e TEAD1-expressing myofiber, suggesting that myofiber-specific TEAD1 overexpression activates a physi

256 his was tested in adult conditional skeletal myofiber-specific VEGF gene-ablated mice (VEGF(HSA-/-) )

257 P extracellular ATP (eATP) released by dying myofibers steadily activates muscle and immune purinergi

258 le for normal stem cell activity in reducing myofiber strain associated with hypertrophy.

259 Finite-element modeling projected myofiber stress reduction (>50%; P<0.001) with dual-cros

260 These findings reinforce the role of elastic myofiber stretch as a growth stimulant at both cellular

261 ropic growth constitutive model with elastic myofiber stretch as the growth stimuli to simulate long-

262 driven by the deviations of maximum elastic myofiber stretch over a cardiac cycle from its correspon

263 tal muscle disorder associated with aberrant myofiber structure and contractility.

264 usly via signal(s) from the TEAD1-expressing myofiber, suggesting that myofiber-specific TEAD1 overex

265 , including an affinity for the postsynaptic myofiber surface and phagocytosis of nerve terminals.

266 ccessfully triggered glycolytic-to-oxidative myofiber switch, increased functional mitochondrial cont

267 rcise by stimulating glycolytic-to-oxidative myofiber switch, mitochondrial biogenesis and angiogenes

268 Skeletal muscles contain heterogeneous myofibers that are different in size and contractile spe

269 Mutant stem cells contribute to hypotrophic myofibers that are not innervated but retain the ability

270 for skeletal muscle, comprised of syncytial myofibers that each accrue hundreds of nuclei during dev

271 Individual myofibers that make up muscle tissue exhibit variation i

272 In the myofiber, Thbs4 selectively enhances vesicular trafficki

273 injury causes significant alterations to the myofiber through a muscle stem cell-mediated accumulatio

274 s promotes myoblast migration to the tips of myofibers through cell-cell contact.

275 chondrial content per myonucleus in ischemic myofibers to compensate for impaired mitochondrial funct

276 lls, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.

277 ecialized transcriptional programming within myofibers, tracking activation-induced transcriptional c

278 ent RNA, we measured a sevenfold increase in myofiber transcription during early hypertrophy before a

279 te transcription during hypertrophy and that myofiber transcription is responsive to DNA content but

280 Although dystrophin deficiency in myofiber triggers the disease's pathological changes, th

281 dystrophy pathogenesis that included reduced myofiber turnover and histopathology, reduced fibrosis,

282 he other hand, cellular localization of slow myofiber-type genes revealed their increased expression

283 Similarly, global expression of slow myofiber-type genes showed upregulation in affected chic

284 r that expresses Pax7 and contributes to all myofiber types.

285 ofibers without affecting the composition of myofiber types.

286 Here we report that skeletal myofiber VEGF directly or indirectly regulates exercise-

287 is region with exercise training or skeletal myofiber VEGF gene deletion.

288 This study demonstrates that skeletal myofiber VEGF is required for the hippocampal VEGF respo

289 Our results found skeletal myofiber VEGF to be necessary for maintaining blood flow

290 chanisms by which exercise, through skeletal myofiber VEGF, affects the hippocampus.

291 n contrast, a decrease in myonuclear domain (myofiber volume/myonucleus) was observed regardless of m

292 RVs and intact myofibers were laser microdissected from skeletal muscle

293 scle structure after injury, as regenerating myofibers were more abundant and myofiber size was large

294 e, and respiration assessed in permeabilized myofibers were not significantly altered in response to

295 n immature myotubes and fully differentiated myofibers, where it forms ectopic MT organizing centers,

296 The ability to image single myofibers will serve as a valuable tool to study MR prop

297 e found that MRM can be used to image single myofibers with 6-mum resolution.

298 duced muscle mass and a higher proportion of myofibers with a smaller cross-sectional area.

299 yofibers, a preparation that isolates single myofibers with their associated muscle stem cells remain

300 of Mettl21e in mice reduced the size of IIb myofibers without affecting the composition of myofiber

301 low succinate dehydrogenase (SDH) expressing myofibers, without a change in the size of MHC IIA posit