ライフサイエンスコーパス: myofiber

1 the even positioning of nuclei in the mature myofiber.

2 ith dystrophin at the sarcolemma in skeletal myofibers.

3 ouse by blunting the regeneration of injured myofibers.

4 er of embryonic myosin-positive regenerating myofibers.

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

6 nflammation or adipogenic replacement of the myofibers.

7 mice lacking ERK1/2 selectively in skeletal myofibers.

8 s, regardless of the orientation of adjacent myofibers.

9 lation, differentiation and cell fusion into myofibers.

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

11 ting the nuclei of terminally differentiated myofibers.

12 hly and specifically expressed in glycolytic myofibers.

13 edominantly contained in fast twitch/type II myofibers.

14 er LSI, well after the appearance of damaged myofibers.

15 flammation and adipogenic replacement of the myofibers.

16 nd C2C12 cells, which can differentiate into myofibers.

17 usion of PMO-loaded myoblasts into repairing myofibers.

18 t from oxidative to glycolytic metabolism in myofibers.

19 ates, differentiates, and fuses with injured myofibers.

20 d increased numbers of central nuclei within myofibers.

21 d increase in the same current in dystrophic myofibers.

22 ion of activated satellite cells to form new myofibers.

23 Wnt7a/Fzd7 signaling complexes to recipient myofibers.

24 e protein accumulations (nemaline bodies) in myofibers.

25 ucleus of developing myocardium and skeletal myofibers.

26 sosomes, given that GAA was expressed within myofibers.

27 ofibers and showed disturbed architecture of myofibers.

28 mproved the membrane stability of dystrophic myofibers.

29 contribution of these cells to regenerating myofibers.

30 ssion and increased the size of regenerating myofibers.

31 cle biopsy samples containing AAT-expressing myofibers.

32 itive vesicles that are expressed throughout myofibers.

33 tivated mainly in muscle progenitors and not myofibers.

34 nment of scaffold nanofibers with endogenous myofibers.

35 h fusion of myoblasts to form multinucleated myofibers.

36 tes fusion of exogenous myoblasts to injured myofibers.

37 nonucleated myoblasts to form multinucleated myofibers.

38 most enriched in exosomes compared to parent myofibers.

39 he extracellular matrix (ECM) that surrounds myofibers.

40 uch-evoked motility, and highly disorganized myofibers.

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

42 n of myoblasts preferentially at the tips of myofibers.

43 pment, myoblasts fuse to form multinucleated myofibers.

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

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

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

47 Microinjury to dystrophic myofibers also causes secondary imbalances in sarcolemmi

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

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

50 Immunostaining of nonpermeabilized myofibers and cardiocytes revealed that some obscurin ki

51 Ang II reduced the number of regenerating myofibers and decreased expression of SC proliferation/d

52 D, expressed primarily by type IId/x and IIa myofibers and enriched at endothelial cells, is induced

53 PD123319 reduced the size of regenerating myofibers and expression of the myoblast differentiation

54 le is composed of both slow-twitch oxidative myofibers and fast-twitch glycolytic myofibers that diff

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

56 ze together with increased residual necrotic myofibers and fat accumulation.

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

58 IB inhibitor produced hypertrophy of type 2b myofibers and modest increases of strength and life span

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

60 fferentially required for the maintenance of myofibers and neuromuscular synapses in adult mice.

61 environment were performed in permeabilized myofibers and primary myotubes prepared from vastus late

62 young mice, with reduced capacity to repair myofibers and repopulate the stem cell reservoir in vivo

63 soas muscles confirmed lipid droplets within myofibers and showed disturbed architecture of myofibers

64 Individual myofibers and tenocytes in Drosophila interact through i

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

66 ed architecture, multinucleated and striated myofibers, and a Pax7(+) cell pool.

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

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

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

70 as left ventricular hypertrophy, disarray of myofibers, and interstitial fibrosis.

71 Hence, our results show that the myofibers are central mediators of the deleterious effec

72 irmed the presence and distribution of these myofiber arrays at the microscopic scale.

73 this approach to resolve intravoxel crossing myofiber arrays in the setting of the human tongue, an o

74 ts that depict the macroscale orientation of myofiber arrays.

75 hese findings were apparent in permeabilized myofibers as well as in primary myotubes.

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

77 Moreover, myofibers at distal sites that fused with Wnt7a-treated

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

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

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

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

82 blasts that managed to fuse with the injured myofibers by days 5 and 7 after notexin injury as compar

83 ive interactions inhibit innervation of slow myofibers by fast motor axons during both postnatal matu

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

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

86 skeletal muscle cell hypertrophy, decreased myofiber central nucleation and increased focal macropha

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

88 individual myoblasts to form multinucleated myofibers constitutes a widely conserved program for gro

89 e composition results in muscles with slower myofiber contraction and relaxation, and also decreases

90 he diaphragm, while increasing its thickness,myofiber count, and myofiber diameter, thereby augmentin

91 Crtc2-overexpressing mice have increased myofiber cross-sectional area, greater intramuscular tri

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

93 is essential for muscle fiber integrity and myofiber cytoarchitecture.

94 erlin-sufficient A/WySnJ mice show much less myofiber damage and inflammation and lesser cytokine lev

95 ically induced sarcolemma disruptions causes myofiber damage and necrosis.

96 We report that myofiber damage in A/J mice occurs before inflammatory c

97 inflammatory macrophage differentiation and myofiber damage in virus-infected skeletal muscle, thus

98 Myofiber damage induced by eccentric strain increased wi

99 and studied the progression of torque loss, myofiber damage, and inflammation afterward.

100 consequence and not the cause of progressive myofiber damage.

101 ally, we show that p38alpha directly induces myofiber death through a mitochondrial-dependent pathway

102 ignaling events that directly participate in myofiber death.

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

104 like macrophages corresponded with increased myofiber degeneration in WT mice.

105 tion in WT macrophages blocked virus-induced myofiber degeneration, and pharmacologic ablation of mac

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

107 scle of the diabetic mice that would lead to myofiber degeneration.

108 characterized by mitochondrial dysfunction, myofiber degradation, and fibrosis in their ischemic leg

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

110 Contractility studies on permeabilized myofibers demonstrated reduced maximal active tension fr

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 in embryonic development and particularly in myofiber development, muscle integrity and activity.

115 functionally mature, evidenced by increased myofiber diameter and improved calcium handling and cont

116 increasing its thickness,myofiber count, and myofiber diameter, thereby augmenting by 72% the amount

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

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

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

120 Thus, myofiber ERK1/2 are differentially required for the main

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

122 fects on the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the st

123 ncluding a reduction in the number of muscle myofibers, even in mild or intermediate phenotype morpha

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

125 Isolated myofibers expressing lacZ were imaged with and without a

126 y and cellular-directed alignment for muscle myofiber fabrication, has raised awareness of their pote

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

128 cles, and misexpression of ephrin-A3 on fast myofibers followed by denervation/reinnervation promotes

129 oes not affect the muscle size and repair of myofibers following focal sarcolemmal injury and lengthe

130 junctions (NMJs) when cocultured with chick myofibers for several weeks.

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

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

133 ice display widespread necrosis and impaired myofiber formation.

134 The sarcolemma of freshly isolated WT myofibers from denervated muscles also showed high hemic

135 e regenerate new vascularized and innervated myofibers from human myogenic precursor cells.

136 Myofibers from muscle-specific STIM1 transgenic mice sho

137 droplets were also conspicuous within human myofibers from patients with dysferlinopathy (but not ot

138 enerate enough muscle cells to sustain fetal myofiber growth.

139 equirement to achieve efficient hypertrophic myofiber growth.

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

141 Myofiber helix angle, mean diffusivity, fractional aniso

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

143 rd adult pre-mRNA splicing patterns, reduced myofiber hypertrophy and a decrease in myonuclear foci c

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

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

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

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

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

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

150 cking ephrin-A3 have dramatically fewer slow myofibers in fast and mixed muscles, and misexpression o

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

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

153 The arrangement of myofibers in the heart is highly complex and must be rep

154 Myofibers in the ventricular septum follow a stereotypic

155 nly the LR2006 OPY1 strain replicated within myofibers in vivo, despite similar growth of the two str

156 at loss of EHD1 leads to smaller muscles and myofibers in vivo.

157 mirrored the pathological features of EBS-MD myofibers, including the presence of desmin-positive pro

158 Myofibers increase size and DNA content in response to a

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

160 omyelitis virus (TMEV) infection of skeletal myofibers induces inflammation and subsequent dystrophic

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

162 Surprisingly, although similar extensive myofiber infection and inflammation are observed in SHP-

163 train was administered directly into muscle, myofiber infection was comparable to that in LR2006 OPY1

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

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

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

167 that they may function similarly to maintain myofiber integrity.

168 air and regeneration of the injured skeletal myofiber involves fusion of intracellular vesicles with

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

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

171 ent as a mediator of unc45b up-regulation in myofibers lacking myosin folding proteins.

172 initiated by unregulated Ca(2+) influx into myofibers leading to their death.

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

174 Increased myofiber length is caused by enhanced myoblast prolifera

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

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

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

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

179 he strain of CHIKV to establish infection in myofibers may contribute to the increased disease severi

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

181 ) mice through a mechanism involving reduced myofiber membrane fragility.

182 roblasts, whereas ezrin colocalized with the myofiber membranes.

183 robably due to alterations of the dystrophic myofiber membranes.

184 that may link meta-inflammation to skeletal myofiber metabolism and insulin resistance.

185 Expression of dnTGFbetaRII in myofibers mitigated the dystrophic phenotype observed in

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

187 Myofiber necrosis and fascial inflammation can be detect

188 dystrophic muscle, which resulted in severe myofiber necrosis and many hallmarks of muscular dystrop

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

190 for ultrasound echogenicity's prediction of myofiber necrosis was 0.74 (95% CI, 0.565 to 0.919; p =

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

192 als displayed progressive muscle damage with myofiber necrosis, internalized nuclei, and, at older ag

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

194 ed fulminant muscle disease characterized by myofiber necrosis, swollen mitochondria, infiltration of

195 these mice neither accumulate dead calcified myofibers nor lose ambulation.

196 Subendocardial myofibers normally run in parallel along the left ventri

197 arkers did not correlate with Ki-67-affected myofiber nuclei.

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

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

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

201 cultured satellite cells and in regenerating myofibers of TWEAK-KO mice.

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

203 diffusional data that defines highly ordered myofiber patterns in architecturally complex tissue.

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

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

206 The myofiber precursor is the nascent myotube, and during my

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

208 in gene expression for fast- and slow-twitch myofiber proteins, and rescued cardiac function in Trbp(

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

210 Furthermore, coincident with delayed myofiber recovery, we observed reduced muscle ATP conten

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

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

213 cle has a unique complement of fast and slow myofibers, reflecting patterns established during develo

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

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

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

217 o role of Anx A1 in cell fusion required for myofiber regeneration and not in intracellular vesicle f

218 1 arm of the UPR in satellite cells inhibits myofiber regeneration in adult mice.

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

220 increases satellite cells proliferation and myofiber regeneration in young mdx mice.

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

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

223 ls was observed and correlated with enhanced myofiber regeneration.

224 maturation of the neuromuscular junction and myofiber reinnervation after injury.

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

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

227 ting that sympathetic outflow also regulates myofiber remodeling.

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 perturbs AMPK activity, resulting in delayed myofiber repair.

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

233 bility of a recent epidemic strain to infect myofibers results in increased disease severity.

234 catenin signaling in the well-differentiated myofibers results in the failure of maintenance of their

235 , which plays a crucial role in connecting a myofiber's cytoskeleton to the surrounding extracellular

236 cellular vesicle fusion needed for repair of myofiber sarcolemma.

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

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

239 dings identify Nur77 as a novel regulator of myofiber size and a potential transcriptional link betwe

240 aminin-111 treatment promoted an increase in myofiber size and number, and an increased expression of

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

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

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

244 xpression, ubiquitin-proteasome activity and myofiber size modulated by PMI5011 in the presence of in

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

246 otoxin) resulted in the smallest regenerated myofiber size together with increased residual necrotic

247 rity, fewer centralized myonuclei, increased myofiber size, and improved muscle physiology and perfor

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

249 the SIRT1 deacetylase domain display reduced myofiber size, impaired muscle regeneration, and derepre

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

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

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

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

254 skeletal muscle in mice led to increases in myofiber size.

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

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

257 Here, we generated transgenic mice with myofiber-specific inhibition of TGFbeta signaling owing

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

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

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

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

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

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

264 PTEN ubiquitination was reduced in DM2 myofibers, suggesting that the NEDD4-PTEN pathway is dys

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 hat leads to the formation of multinucleated myofibers, syncytiotrophoblasts and osteoclasts, allowin

269 rogels yielded a higher number of functional myofibers than cells that were cultured on hydrogels wit

270 idative myofibers and fast-twitch glycolytic myofibers that differentially impact muscle metabolism,

271 In the myofiber, Thbs4 selectively enhances vesicular trafficki

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

273 omplex, a laminin receptor that connects the myofiber to its surrounding extracellular matrix.

274 muscles within the hand and then relocate as myofibers to their final position in the arm.

275 he ability of injected cells to generate new myofiber tracts and provided a fundamental readout of th

276 tional anisotropy, and the appearance of new myofiber tracts with the correct orientation.

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

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

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

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

281 f postnatal "matching" whereby predetermined myofiber type identity promotes pruning of inappropriate

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

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

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

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

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

287 contractile properties in dissected patient myofibers was measured.

288 RVs and intact myofibers were laser microdissected from skeletal muscle

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

290 e ligand ephrin-A3 is expressed only on slow myofibers, whereas its candidate receptor, EphA8, locali

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

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

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

294 paired regeneration characterized by smaller myofibers with increased centrally localized nuclei and

295 A muscle biopsy revealed scattered myofibers with internal nuclei, atrophy, and regeneratio

296 used insults that primarily affect only the myofibers without affecting the muscle tissue microenvir

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

298 ventricular myofiber work than with LV or RV myofiber work alone.

299 max correlated better with total ventricular myofiber work than with LV or RV myofiber work alone.

300 ns, LVP and BiVP increased total ventricular myofiber work to the same extent.