ライフサイエンスコーパス: mdx mice

1 eased muscle damage when compared to regular mdx mice.

2 injury and increases fibrosis in 9-month-old mdx mice.

3 n inflammation in the fore- and hindlimbs of mdx mice.

4 tent or oxidative phosphorylation defects in mdx mice.

5 avates nor alleviates cardiomyopathy in aged mdx mice.

6 by activity (ie, voluntary wheel running) in mdx mice.

7 rdiomyopathy matching that of non-transgenic mdx mice.

8 from decreased mitochondrial dysfunction in mdx mice.

9 irror the progression of muscle pathology in mdx mice.

10 ogenic gene expression compared with control mdx mice.

11 rcise muscle damage, hypoxia, and fatigue in mdx mice.

12 s some components of dystrophic pathology in mdx mice.

13 ceptibility to contraction-induced injury in mdx mice.

14 rin and negligible additional improvement in mdx mice.

15 ly compensates for the loss of dystrophin in mdx mice.

16 e morpholino targeting exon 23 in dystrophic mdx mice.

17 ed eccentric contractions when compared with mdx mice.

18 nd myofiber hypertrophy in treated mucles in mdx mice.

19 in the heart and increased cardiac damage in mdx mice.

20 follow disease progression in the hearts of mdx mice.

21 cue by dystrophin and utrophin constructs in mdx mice.

22 d to primary muscle cells from wild type and mdx mice.

23 ed improved heart function in Mmp9-deficient mdx mice.

24 s of MMP-9 in cardiac and skeletal muscle of mdx mice.

25 ion of ERK1/2 and Akt kinase in the heart of mdx mice.

26 ventricle dilation, and fibrosis in 1-y-old mdx mice.

27 exacerbates myopathy in dystrophin-deficient mdx mice.

28 evels of MMP-9 are increased in the heart of mdx mice.

29 pression of MMP-3 and MMP-12 in the heart of mdx mice.

30 show more severe muscle phenotypes than the mdx mice.

31 ctivity in Duchenne muscular dystrophy (DMD) mdx mice.

32 ases and activator protein-1 in myofibers of mdx mice.

33 ically distinct model of muscular dystrophy, mdx mice.

34 nic myosin heavy chain in skeletal muscle of mdx mice.

35 flow and force production, compared with the mdx mice.

36 e-related cardiac dysfunction present in the mdx mice.

37 are down-regulated, in dystrophic muscle of mdx mice.

38 rovements in muscle strength and function in mdx mice.

39 ta-dystroglycan and neuronal nitric oxide in mdx mice.

40 ugmented the skeletal muscle regeneration in mdx mice.

41 enesis and enhanced myofiber regeneration in mdx mice.

42 ion into muscle fibers in muscular dystrophy mdx mice.

43 l dystrophin protein in dystrophin-deficient mdx mice.

44 nt within the dystrophic skeletal muscles of MDX mice.

45 ent systemic dystrophin splice correction in mdx mice.

46 ion of delta-Dko mice was worse than that of mdx mice.

47 ficantly improved hind limb grip strength in mdx mice.

48 nction and increased exercise performance in mdx mice.

49 nsforming growth factor-beta in myofibers of mdx mice.

50 expression of MMP-9 in dystrophic muscle of mdx mice.

51 -micro-dystrophin (AAV-muDys) to young adult mdx mice.

52 drastically increased in skeletal muscle of mdx mice.

53 tical role in ameliorating muscle disease in mdx mice.

54 tein causes myopathy in dystrophin-deficient mdx mice.

55 expressed in muscles of dystrophin-deficient mdx mice.

56 on also contributes to the mild phenotype in mdx mice.

57 greatly reduced by null mutation of MBP-1 in mdx mice.

58 s muscular dystrophy in dystrophin-deficient mdx mice.

59 sion and reduce overall disease pathology in mdx mice.

60 in improved pathology and muscle function in mdx mice.

61 curvature between patches from wild-type and mdx mice.

62 ffects of transgenic PGC-1alpha in muscle of mdx mice.

63 iated muscle cells from dystrophin-deficient mdx mice.

64 disease phenotype is more severe than in B10-mdx mice.

65 agation was not different between normal and mdx mice.

66 may be sufficient to treat cardiomyopathy in mdx mice.

67 digitorum brevis (FDB) muscles of normal and mdx mice.

68 ragm muscle fibers from dystrophin-deficient mdx mice.

69 imilar between control-fed and quercetin-fed mdx mice.

70 mal nNOSmu on muscle contractile function in mdx mice.

71 stores under energy-deficient conditions in mdx mice.

72 at their pathology is different from the B10-mdx mice.

73 e-dependent changes of diaphragm function in mdx mice.

74 (10%) was found after Alk4 AON treatment in mdx mice.

75 ed cardiac function, relative to age-matched mdx mice.

76 gnificantly altered (P < 0.001, q < 0.01) in mdx mice.

77 old) and old (~14-months old) wild type and mdx mice.

78 he muscles of periodate-oxidized ATP-treated mdx mice.

79 tage of regenerating fibers and fibrosis) in mdx mice.

80 mpensatory mechanism for the loss of nNOS in mdx mice.

81 muscle cell progenitors expressing Pax 7 in mdx mice.

82 ible to contraction-induced muscle damage in mdx mice.

83 pathology, inflammation, and dysfunction in mdx mice.

84 in muscles of periodate-oxidized ATP-treated mdx mice.

85 irs both autophagy and lysosome formation in mdx mice.

86 gy and Akt signaling in dystrophic muscle of mdx mice.

87 ear factor-kappa B (NF-kappaB) in 7-week-old mdx mice.

88 grip strength by 60-80% over vehicle-treated mdx mice.

89 he skeletal and cardiac disease phenotype in mdx mice.

90 generally more severely affected than dy(3K)/mdx mice.

91 iferation and myofiber regeneration in young mdx mice.

92 teomes of wild-type and dystrophin-deficient mdx mice.

93 ic muscle phenotype in dystrophin deficient (mdx) mice.

94 not in others such as dystrophin-deficient (mdx) mice.

95 tion and cause muscle fatigue in dystrophic (mdx) mice.

96 and enhanced muscle function in dystrophic (mdx) mice.

97 Treatment of mdx mice (a DMD model) with R16/17-containing synthetic

98 Studies performed in young adult mdx mice (a mild DMD mouse model) have yielded opposing

99 In one-year-old mdx mice (a model for Duchenne muscular dystrophy, DMD),

100 d prevents functional ischemia in transgenic mdx mice, a DMD model.

101 tory and antifibrotic effects of imatinib in mdx mice, a DMD mouse model.

102 phin gene (Dmd) mutation in the germ line of mdx mice, a model for DMD, and then monitored muscle str

103 ration and function of dystrophic muscles in mdx mice, a model for Duchenne muscular dystrophy.

104 9 mini-dystrophin gene in skeletal muscle of mdx mice, a model for Duchenne muscular dystrophy.

105 N in Duchenne muscular dystrophy (DMD) using mdx mice, a model of DMD, and by generating transgenic m

106 immunological milieu of dystrophic muscle in mdx mice, a model of DMD, to identify potential therapeu

107 tion reduces aberrant Ca(2+) influx in young mdx mice, a model of DMD.

108 contributes to the increased fatigability of mdx mice, a model of DMD.

109 appaB was sufficient to improve pathology in mdx mice, a model of DMD.

110 lowing acute muscle injury or in muscle from mdx mice, a model of DMD.

111 deliver gene-editing components to postnatal mdx mice, a model of DMD.

112 grafted into muscles of dystrophin-deficient mdx mice, a model of Duchenne muscular dystrophy (DMD).

113 lling and necrotic disease manifestations in mdx mice, a model of Duchenne muscular dystrophy, and in

114 pproaches that rescue defective autophagy in mdx mice, a model of Duchenne muscular dystrophy, with t

115 injury have not been extensively studied in mdx mice, a murine model of Duchenne muscular dystrophy

116 ensor digitorum longus muscles in dystrophic mdx mice, a murine model of Duchenne muscular dystrophy.

117 livered to the heart of ~14-month-old female mdx mice, a phenotypic model of Duchenne cardiomyopathy.

118 dampened the local inflammatory response in mdx mice, a spontaneous mouse model of dystrophin defici

119 has not been described in DMD patients or in mdx mice, a widely used mouse model for studying DMD.

120 We assayed whether ablation of IL-10 in mdx mice affected satellite cell numbers, using Pax7 exp

121 und that delaying exogenous Akt treatment of mdx mice after the onset of peak pathology (>6 weeks) si

122 Genetic ablation of the iNOS gene in mdx mice also significantly reduces muscle membrane lysi

123 dystrophy, the Y890F mice were crossed with mdx mice an established model of muscular dystrophy.

124 between muscular dystrophy and vasculature, mdx mice, an animal model for DMD, were crossed with Flt

125 Skeletal muscle gene expression profiles of mdx mice, an animal model of DMD, treated with prednisol

126 se oligonucleotide-mediated exon-skipping in mdx mice and (2) stable restoration of alpha-sarcoglycan

127 and function were made in the same group of mdx mice and controls (housed in a non-SPF facility) usi

128 mice but unchanged in TA muscles of treated mdx mice and diaphragm of treated mdx and dko mice.

129 In mdx mice and Duchenne muscular dystrophy patients, dystr

130 Dystrophin-deficient mdx mice and dystrophin/utrophin double-knockout (dKO) m

131 c, nNOS transgene increases the endurance of mdx mice and enhances glycogen metabolism during treadmi

132 nted the progressive ventricular fibrosis of mdx mice and greatly reduced myocarditis.

133 hat SSPN overexpression is well tolerated in mdx mice and improves sarcolemma defects that underlie s

134 enuates the muscular dystrophic phenotype in mdx mice and may be a potential therapeutic target in mu

135 N was substantially elevated in the serum of mdx mice and muscle biopsies after disease onset.

136 ction would decrease calcium influx in adult mdx mice and that MEMRI would be able to monitor and dif

137 erformance deficits, and gait anomalies than mdx mice and that these deficits began at a younger age.

138 he impact of the disease on the life span of mdx mice and the cause of death remain unresolved.

139 gammadelta T cells to the cardiac muscle of mdx mice and to characterize their phenotype and functio

140 Muscles of both mdx mice and very old rats showed major reductions in th

141 In contrast, for muscles of mdx mice and very old rats, forces transmitted laterally

142 old) and old (~14-months old) wild type and mdx mice, and human Abductor Hallucis (AH) and gastrocne

143 ed in the skeletal muscle of dKO mice versus mdx mice, and RhoA activation specifically occurred at t

144 evated in muscles from dystrophin-deficient (mdx) mice, and mdx/Stra13-/- double mutants exhibit an e

145 The mdx mice are a model for the human disease, Duchenne mus

146 contrast to human patients, dystrophin-null mdx mice are only mildly affected.

147 We found unexpectedly that patches from mdx mice are strongly curved towards the pipette tip by

148 Akt also improves muscle function in mdx mice as demonstrated through in vivo grip strength t

149 obutamine stress was identified in the RV of mdx mice as early as 1 month.

150 identify cardiac abnormalities in the RV of mdx mice as young as 1 month, and detected myocardial fi

151 4 weeks of age did not influence fibrosis in mdx mice, as determined by measuring hydroxyproline leve

152 ted fibrogenesis and muscle deterioration in mdx mice, as well as exacerbated dystrophy in young PAI-

153 so restored dystrophin protein expression in mdx mice at 6 wk after cell treatment that was further i

154 to distinguish between the WT wild type and mdx mice at any time point.

155 rom wild-type, integrin alpha7-deficient and mdx mice at birth, but died within 24-28 days.

156 ator of cellular metabolism and survival, in mdx mice at pre-necrotic (<3.5 weeks) ages and demonstra

157 M2 phenotype and improved motor function of mdx mice at that later stage of the disease.

158 e in vivo or improve gross motor function of mdx mice at the early, acute peak of pathology.

159 nistration, and was 26% greater than control mdx mice at this time.

160 In 6-week-old mdx/mdx mice, blood leukocytes, including T cells, were CD62

161 We found dilated cardiomyopathy in old mdx mice but not in age-matched carrier mice.

162 trophic symptoms in the limb muscle of young mdx mice, but did not prevent degeneration and regenerat

163 the diaphragm of mdx((5)cv) mice compared to mdx mice, but similar force generation in the extensor d

164 We also show that eosinophil depletions of mdx mice by injections of anti-chemokine receptor-3 redu

165 er cardiac pathology in dystrophin-deficient mdx mice can be corrected by the elevated production of

166 sed fibrosis in skeletal muscle fibers of D2-mdx mice compared with B10-mdx and control.

167 traction was increased in batimastat-treated mdx mice compared with those treated with vehicle alone.

168 ac contractility and caused 95% mortality in mdx mice, contractility was preserved with only 19% mort

169 as exacerbated dystrophy in young PAI-1(-/-) mdx mice, could be reversed by miR-21 or uPA-selective i

170 we quantified muscular dystrophy measures in mdx mice deleted for Galgt2 (Galgt2(-/-)mdx).

171 Compared with WT mice, motor end-plates of mdx mice demonstrated less continuous morphology, more d

172 mdx mice, we created dystroglycan transgenic mdx mice (DG/mdx).

173 In mdx mice, diaphragm amplitude decreased with age and val

174 (dKO) mice are mouse models of DMD; however, mdx mice display a strong muscle regeneration capacity,

175 emetry of freely ambulatory mice showed that mdx mice displayed cardiac abnormalities that are charac

176 ion, the dystrophin-null heart of transgenic mdx mice displayed severe cardiomyopathy matching that o

177 , in comparison to young-adult (3-month-old) mdx mice displaying only mild muscle lesions with no fib

178 ime, our study focused on old (12-month-old) mdx mice, displaying marked chronic muscle lesions, simi

179 ost normal in young-adult in contrast to old mdx mice, displaying marked microvessel alterations, and

180 wn-regulated (50-85%) in skeletal muscles of mdx mice (DMD model) vs. wild-type mice.

181 Since mdx mice do not develop dystrophic cardiomyopathy until

182 be established because young dystrophin-null mdx mice do not have heart disease.

183 but these cells were found in the hearts of mdx mice during the study period, reaching a peak in 12-

184 cells (MDSCs) transplanted into dystrophic (mdx) mice efficiently regenerate skeletal muscle.

185 addition, conditional deletion of IKKbeta in mdx mice elucidated that NF-kappaB functions in activate

186 As with mdx mice, embryonic overexpression of the Galgt2 transge

187 of dystrophin deficiency on nNOSbeta and use mdx mice engineered to lack nNOSmu and nNOSbeta to disce

188 Fibers derived from ES cells of mdx mice exhibit an abnormal branched phenotype resembli

189 ted a 36% loss in torque about the ankle but mdx mice exhibited a greater torque loss of 73% (P < 0.0

190 While vehicle-treated castrated mdx mice exhibited cardiopulmonary impairment and fibros

191 In contrast, TA muscles from gsg(-/-) and mdx mice exhibited heightened P-ERK1/2 and increased nuc

192 We show that transgenic mdx mice expressing a full-length dystrophin/utrophin ch

193 ons to chronic myotendinous strain injury in mdx mice expressing a microdystrophin transgene (micrody

194 tion in primary muscle cells from humans and mdx mice expressing dystrophin nonsense alleles, and res

195 elevated to that of mdx levels in transgenic mdx mice expressing nearly full-length dystrophin.

196 Treatment of mdx mice for 4 weeks with an established AMPK agonist, A

197 d Cx43 function prior to challenge protected mdx mice from arrhythmogenesis and death, while mdx:utr

198 In contrast to results discussed in mdx mice, genetic deletion of a loxP-targeted calcineuri

199 Myocytes from mdx mice had a higher incidence of isoproterenol-induced

200 The 9-month-old mdx mice had elevated Penh values and decreased breathin

201 Galgt2(-/-) mdx mice had increased heart and skeletal muscle patholo

202 As expected, transgenic mdx mice had minimal skeletal muscle disease and they al

203 for Duchenne muscular dystrophy patients and mdx mice has proven to be a safe but ineffective form of

204 However, unlike patients with DMD, mdx mice have a very mild motor function deficit, posing

205 s or their cell extracts into the muscles of mdx mice (i.e., a mouse model of Duchenne Muscular Dystr

206 Conversely, weekly steroid treatment in mdx mice improved muscle function and histopathology and

207 Deletion of Mmp9 gene in mdx mice improved skeletal muscle structure and function

208 reduces muscle membrane lysis in 4-week-old mdx mice in vivo.

209 Ablation of IL-10 expression in mdx mice increased muscle damage in vivo and reduced mou

210 r, over-expression of nNOS in the muscles of mdx mice increased serum NO and normalized cell prolifer

211 In mdx mice, increased m-calpain levels in dystrophic soleu

212 ounced latency to activation in patches from mdx mice is caused by the mechanical relaxation time req

213 Diaphragm function in mdx mice is commonly evaluated by specific force measure

214 -null (Sgcd(-/-)) mice and dystrophin mutant mdx mice is dramatically improved by skeletal muscle-spe

215 The inward curvature of patches from mdx mice is eliminated by actin inhibitors.

216 roves muscle structure and function in young mdx mice, its continued inhibition causes more severe my

217 Intriguingly, in the skeletal muscle of mdx mice lacking dystrophin, we discover that the expres

218 nerative myogenesis and dystrophin-deficient mdx mice lacking Mkp5 exhibited an attenuated dystrophic

219 attenuation of dystrophic features found in mdx mice lacking myostatin.

220 We report that mdx mice lacking the RNA component of telomerase (mdx/mT

221 il >/=21 months of age, we reasoned that old mdx mice may represent a better model to assess the impa

222 In mdx mice, MKP-1 deficiency reduced body weight, muscle m

223 taking advantage of Flk1(GFP/+) crossed with mdx mice (model for human DMD where all blood vessels ex

224 In mdx mice, mSSPN overexpression improves dystrophic patho

225 Mechanical anisotropy in WT wild type and mdx mice muscle were compared by using t test and one-wa

226 In dystrophic humans and mdx mice, mutations in the dystrophin gene disrupt the s

227 disease and they also outperformed original mdx mice on treadmill running.

228 d the EMG measures decreased after injury in mdx mice only.

229 f two members of this complex, dystrophin in mdx mice or alpha sarcoglycan in Sgca(-/-) mice, results

230 ed in collagen deposition, either decreased (mdx mice) or increased (C57BL/10 mice) after double CD4/

231 a model of DMD, and by generating transgenic mdx mice overexpressing ApN.

232 ls exert protective effects on the hearts of mdx mice, possibly by selectively killing pathogenic mac

233 nNOS depletion from mdx mice prevented compensatory skeletal muscle cell hyp

234 However, ablation of MBP-1 expression in mdx mice produces other effects on muscular dystrophy.

235 ngrafted into muscle of dystrophin-deficient mdx mice, purified SMPs contributed to up to 94% of myof

236 vels in the serum), which in 12-week-old mdx/mdx mice reduces blood T cell competence to adhere to ca

237 ent vastly improved overall muscle health in mdx mice, reducing plasma creatine kinase activity, an e

238 ine kinase activity were not decreased in DG/mdx mice relative to mdx animals.

239 isms leading to increased levels of MMP-9 in mdx mice remain unknown.

240 letal muscle compared with the wild-type and mdx mice, respectively.

241 selectively in the dystrophic muscles of the mdx mice restored metabolic and angiogenic gene expressi

242 Expression of a klotho transgene in mdx mice restored their longevity, reduced muscle wastin

243 PNADMD into the tibealis anterior muscles of mdx mice resulted in approximately 3-fold higher numbers

244 erodimer and that increasing beta1D chain in mdx mice results in more functional integrin at the sarc

245 Analysis of sera from 1 week to 7 months old mdx mice revealed age-dependent changes in the level of

246 Like humans, dystrophin-deficient mice (mdx mice) show cardiac dysfunction as evidenced by a dec

247 Dag1(Y890F/Y890F)/mdx mice showed a significant improvement in several par

248 In addition, D2-mdx mice showed fewer central myonuclei and increased ca

249 We found that D2-mdx mice showed significantly reduced skeletal muscle fu

250 In mdx mice SR8278 increased lean mass and muscle function,

251 Ca(2+) leak and attenuated cardiomyopathy in mdx mice, suggesting that enhanced PKA phosphorylation o

252 ct was not observed in dystrophin-deficient (mdx) mice, suggesting that accelerated degeneration indu

253 Compared with mdx mice that developed age-dependent heart failure, mdx

254 in nNOS transgenic muscles and muscles from mdx mice that express the nNOS transgene.

255 ildtype mice, which was in stark contrast to mdx mice that had a 55% reduction in M-wave RMS (P < 0.0

256 letal myocytes cultured from wild-type mice, mdx mice that lack the cytoskeletal linkage protein dyst

257 ency happens between 3 and 8 weeks of age in mdx mice, the animal model of DMD.

258 In AICAR-treated mdx mice, the exaggerated sensitivity of mdx diaphragm m

259 In dystrophin-deficient mdx mice, the expression and membrane localization of CA

260 myocardial fibrosis in 6, 9 and 12-month-old mdx mice, the extent of fibrosis correlating with the de

261 imal models of DMD: (i) dystrophin-deficient mdx mice, the most commonly utilized model of DMD, which

262 In untreated mdx mice, the usual effect of muscle contraction to atte

263 an SSPN is expressed at three-fold levels in mdx mice, this increase in adhesion complex abundance im

264 muscle-specific micro-dystrophin transgenic mdx mice to 23 months and examined the cardiac phenotype

265 administered quercetin (0.2%) in 2 month old mdx mice to improve respiratory function and end-point f

266 In mdx mice treated with a peptide-conjugated phosphorodiam

267 In mdx/mdx mice treated with Brilliant Blue G, a P2X7 blocker,

268 or muscles of 2-day-old dystrophin-deficient mdx mice using recombinant adeno-associated viral vector

269 evidence that dilated cardiomyopathy in old mdx mice was prevented by mosaic dystrophin expression o

270 glycan itself inhibits muscular dystrophy in mdx mice, we created dystroglycan transgenic mdx mice (D

271 In mdx mice, we found that overexpression of BCL2 failed to

272 In contrast to age-matched mdx mice, we observed that both the number and regenerat

273 Reductions in muscle integrity in nNOS-null mdx mice were accompanied by decreases in specific force

274 Diaphragm movement amplitude values for mdx mice were considerably lower than those for wild-typ

275 Mdx mice were crossed to ones with cardiac myocyte-speci

276 mdx mice were crossed with RyR2-S2808A mice, in which PK

277 Beginning at 8 weeks of age, mdx mice were fed a standard diet supplemented with 1% s

278 All of these ECG abnormalities in mdx mice were improved or corrected by nNOS transgene ex

279 Dystrophin-deficient mdx mice were produced in which there was myocardial exp

280 Surprisingly, old mdx mice were prone to develop muscle tumors that resemb

281 etermine their therapeutic value, dystrophic mdx mice were subject to forced exercise to model the DM

282 eta signaling improves respiratory function, mdx mice were treated from 2 weeks of age to 2 months or

283 ion compared to myoblasts from wild type and mdx mice, whereas the dko mice show histological abnorma

284 In the hearts of mature Mdx mice (which have a point mutation in Dmd)-a model of

285 transplantation into the skeletal muscle of mdx mice, which model Duchenne muscular dystrophy.

286 ular miRNA signature in dystrophin-deficient mdx mice, which shows profound dose-responsive restorati

287 ed by EOM SCs isolated from dystrophin-null (mdx) mice, while SCs from muscles affected by dystrophin

288 d mdx mice with ApN knockout mice, to obtain mdx mice with ApN depletion.

289 in, we took an opposite approach and crossed mdx mice with ApN knockout mice, to obtain mdx mice with

290 improved muscle histology compared with the mdx mice with decreased fibrosis, calcification and memb

291 We treated mdx mice with intraperitoneal injections of imatinib at

292 We then crossed mdx mice with mice null for caspase-12, the murine equiv

293 Treatment of mdx mice with morpholino oligomers to induce exon skippi

294 +) transients was significantly decreased in mdx mice with no measured difference in that of the surf

295 in and pharmacologic treatment of dystrophic mdx mice with recombinant osteoprotegerin muscles.

296 Finally, in old mdx mice with severe muscle degeneration, simvastatin en

297 s were dramatically reduced in Sgcd(-/-) and mdx mice with the SERCA1 transgene, which also rescued t

298 scles and cardiac tissue in adult dystrophic mdx mice, with a single low-dose injection of peptide-co

299 deficits in the cardiac performance of aged mdx mice, with no effect on normal cardiac function in W

300 les, and rescued striated muscle function in mdx mice within 2-8 weeks of drug exposure.