ライフサイエンスコーパス: nerve injury

1 ll myelination and myelin regeneration after nerve injury.

2 tor CREB in the injured DRG after peripheral nerve injury.

3 riving from hindpaw inflammation or hindlimb nerve injury.

4 ensitization of nociceptors after peripheral nerve injury.

5 tially support motoneuron regeneration after nerve injury.

6 le and female mice, neither before nor after nerve injury.

7 hree well-established rodent models of optic nerve injury.

8 lexor hallucis longus (FHL) tendon may cause nerve injury.

9 R became upregulated in RGCs following optic nerve injury.

10 and that it is increased in adult mice after nerve injury.

11 d a unique role for calcineurin in SCs after nerve injury.

12 ntion of neuropathology after trauma-induced nerve injury.

13 c and inflammatory pain following peripheral nerve injury.

14 ey cellular metabolite, NAD+, in response to nerve injury.

15 can support axon regeneration in peripheral nerve injury.

16 through inhibitory molecules associated with nerve injury.

17 mouse SC development, adult homeostasis, and nerve injury.

18 axon regeneration in patients with traumatic nerve injury.

19 n is essential for recovery after peripheral nerve injury.

20 vioral alterations resulting from peripheral nerve injury.

21 l myelination, but not to proliferate, after nerve injury.

22 ry for mechanical hypersensitivity following nerve injury.

23 n regeneration and functional recovery after nerve injury.

24 e effect on pain hypersensitivity induced by nerve injury.

25 al morphologic activation of microglia after nerve injury.

26 mulate repair in myelin disease or following nerve injury.

27 recruitment, and axon regeneration following nerve injury.

28 ity of myelinated sensory axons that follows nerve injury.

29 ng their actions in neuronal cell death upon nerve injury.

30 es in a neuropathic pain model of peripheral nerve injury.

31 is a determinant of outcome after peripheral nerve injury.

32 rrb2 reverses chronic neuropathic pain after nerve injury.

33 RGCs) promotes axon regeneration after optic nerve injury.

34 ion and functional recovery after peripheral nerve injury.

35 from acute to chronic pain after peripheral nerve injury.

36 plexes were delivered to DRG neurons without nerve injury.

37 axon-to-soma retrograde signaling following nerve injury.

38 nerve and their dynamics after demyelinating nerve injury.

39 actors maintain active enhancer status after nerve injury.

40 he development of heat hyperalgesia after L5 nerve injury.

41 natomic and functional consequences of optic nerve injury.

42 and elongation of axon re-growth after optic nerve injury.

43 n A1R sensitivity in lamina II neurons after nerve injury.

44 l summation in layer 5 ACC neurons following nerve injury.

45 C survival and axon regeneration after optic nerve injury.

46 ic pain-like symptoms even in the absence of nerve injury.

47 for activation of autophagy after peripheral nerve injury.

48 ranslate to improve motor recovery following nerve injury.

49 mice concurrent with axon degeneration after nerve injury.

50 uld promote robust axon regrowth after optic nerve injury.

51 hway, enhanced axon regeneration after optic nerve injury.

52 hronic neuropathic pain following peripheral nerve injury.

53 horn of the spinal cord following traumatic nerve injury.

54 itivity in pain processing in the absence of nerve injury.

55 IRF8-driven reactive microglia in peripheral-nerve injury.

56 of both sexes and in two models of traumatic nerve injury.

57 nd maintaining neuromuscular endplates after nerve injury.

58 n remains sensitive to intrathecal NPY after nerve injury.

59 ion in a clinically relevant model of facial nerve injury.

60 of their electrophysiological function after nerve injury.

61 nd thermal hypersensitivity after peripheral nerve injury.

62 tinal ganglion cells in vivo following optic nerve injury.

63 bule regulation in branch regeneration after nerve injury.

64 ological in neurodegenerative conditions and nerve injuries.

65 stently observed in glaucoma and other optic nerve injuries.

66 g in excitatory neurons following peripheral nerve injuries.

67 therapies to improve outcomes of peripheral nerve injuries.

68 were retrogradely-labeled from muscle before nerve injuries.

69 gical diseases such as stroke and peripheral nerve injuries.

70 (95%CI):0.53 (0.35-0.83), P =.005], cranial nerve injury [0.4% vs.2.7%, RR(95%CI):0.14(0.08-0.23), P

71 ents had higher rates of recurrent laryngeal nerve injury (13.4% vs 6.6%), unplanned reoperations (4.

72 it MNK-eIF4E activity in animals with spared nerve injury, a model of peripheral nerve injury (PNI)-i

73 Peripheral nerve injury accounts for roughly 2.8% of all trauma pat

74 toperative myocardial infarction and cranial nerve injury after TCAR compared to CEA, with no differe

75 Nerve injury also upregulated CSF1 in motoneurons, where

76 eat ENL aiming to prevent the development of nerve injuries and deformities in leprosy.

77 ntly delays axonal degeneration from various nerve injuries and in multiple species; however, the mec

78 ation is a major feature of neuropathies and nerve injuries and occurs via a cell autonomous self-des

79 readily dedifferentiate following peripheral nerve injury and become repair cells.

80 iodorsal thalamus (MD) to ACC, using sciatic nerve injury and chemotherapy-induced mouse models of ne

81 Using a well-known form of nerve injury and combining behavioral analysis, calcium

82 cers as a function of cell type-specificity, nerve injury and development.

83 gainst ER stress, in mouse models of sciatic nerve injury and found that ablation of the transcriptio

84 pace and degree of nerve regeneration after nerve injury and hindlimb transplantation.

85 y ganglia are activated by numerous types of nerve injury and inflammation.

86 ing triggers cold allodynia and up-regulates nerve injury and inflammatory markers in dorsal root gan

87 normal muscle fiber reinnervation following nerve injury and its promotion might mitigate neuromuscu

88 cortical circuits also accompany peripheral nerve injury and may represent additional therapeutic ta

89 n the dorsal horn associated with peripheral nerve injury and pain.

90 e imaging techniques to diagnose and monitor nerve injury and regeneration are being developed, and h

91 molecular mechanisms involved in pain, itch, nerve injury and regeneration.

92 A detailed background of peripheral nerve injury and repair pathology, and an in-depth look

93 ession increased in end target muscles after nerve injury and repair.

94 cular junction (NMJ) reinnervation following nerve injury and repair.

95 GTPases in the Schwann cell (SC) response to nerve injury and repair.

96 ng both development and following peripheral nerve injury and repair.

97 ral nerve can mimic the effect of peripheral nerve injury and significantly increase the number of se

98 2 expression is upregulated after peripheral nerve injury and that Celf2 mutant mice are defective in

99 long-distance axon regeneration after optic nerve injury and uncover a novel and important KLF9-JNK3

100 nced severe hypocalcemia had higher rates of nerve injury and unexpected reoperations, indicating sur

101 peralgesia gradually developed after sciatic nerve injury, and by the last day of testing, THC signif

102 reduces pathologic pain after inflammation, nerve injury, and cancer but not baseline pain.

103 that cold allodynia induced by inflammation, nerve injury, and chemotherapeutics is abolished in mice

104 aviours did not develop in all strains after nerve injury, and correlated only modestly with degree o

105 in RGCs, including in a mouse model of optic nerve injury, and show that the same pathway is active i

106 Runx2, a transcription factor induced after nerve injury, and we show that Runx2 is required for act

107 adaptor protein DAP12 was required for both nerve injury- and intrathecal CSF1-induced upregulation

108 ensitivity in the mouse models of peripheral nerve injury- and paclitaxel-induced neuropathic pain.

109 Although tissue and nerve injuries are well-described causes of pain hyperse

110 contrast, enhancers that lose H3K27ac after nerve injury are enriched for binding sites of the Sox10

111 ying the diminished MOR expression caused by nerve injury are not clear.

112 er with augmented tearing rate after corneal nerve injury, are largely due to upregulation of TRPM8 i

113 actors as important regulators of tumor- and nerve injury-associated pain.

114 pattern and are upregulated following optic nerve injury, but the presence of Nogo-A does not inhibi

115 Peripheral nerve injuries can be extremely debilitating, resulting

116 Peripheral nerve injury can occur in patients with COVID-19 seconda

117 essential motor circuits after a peripheral nerve injury can result in permanent motor deficits due

118 Peripheral nerve injury can trigger neuropathic pain in adults but

119 Chronic pain after arthritis, nerve injury, cancer, and chemotherapy is associated wit

120 IGNIFICANCE STATEMENT Peripheral and central nerve injuries cause life-long disabilities due to the f

121 Nerve injury causes a long-lasting reduction in K(+) cha

122 Our findings demonstrate that a peripheral nerve injury causes activated microglia within reward ci

123 Nerve injury causes down-regulation of MORs in the dorsa

124 However, how nerve injury causes this downregulation is still elusive

125 xia in a mouse model of traumatic peripheral nerve injury, causing painful mononeuropathy.

126 Axonal degeneration (AxD) following nerve injury, chemotherapy, and in several neurological

127 n acute slices showed that, 1 week after the nerve injury, cholinergic modulation of layer 5 (L5) pyr

128 glion neurons using two models of peripheral nerve injury: chronic constriction injury (CCI) and spin

129 Cranial nerve injury (CNI) was 5.5% in the CEA group, while CAS

130 ption factors induced early after peripheral nerve injury confer the cellular plasticity required for

131 Nerve injury consistently increased the enrichment of th

132 CK2alpha's appearance in axons after PNS nerve injury correlates with disassembly of axonal G3BP1

133 to enhance Schwann cell reprogramming after nerve injury could be used to foster effective remyelina

134 ed maintenance of peripheral axons following nerve injury, demonstrating a role for TMEM184b in axon

135 Following nerve injury, denervated Schwann cells (SCs) convert to

136 evoked behaviors or real-time aversion after nerve injury despite marked hypersensitivity to punctate

137 cells, whether transplanted before or after nerve injury, develop into inhibitory neurons, are activ

138 In conclusion, medial and lateral plantar nerve injuries did not occur more frequently, even after

139 orsal horn of the spinal cord in response to nerve injury drives neuropathic pain by selectively acti

140 Nerve injury elicits changes in the expression of genes

141 Following nerve injury, exon methylation is increased, and splicin

142 In mice lacking Ehmt2 in DRG neurons, nerve injury failed to reduce the expression level of MO

143 the primary sensory cell body for peripheral nerve injury generated hypersensitivity, and monitored e

144 icroglia around motoneurons axotomized after nerve injuries has been intensely debated.

145 r versus sensory nerve grafting after facial nerve injury has not been previously investigated.

146 the S1 cortex appears within days following nerve injury; however, the underlying cellular mechanism

147 In this study, we performed optic nerve injury in adult naked mole-rats, the longest livin

148 ubstantially inhibits myelin clearance after nerve injury in both male WT and Ccr2(-/-) mice, highlig

149 s the pathways that contribute to peripheral nerve injury in DN.

150 s required for pain-like responses following nerve injury in mice, and a potential therapeutic target

151 After nerve injury in mice, miR-21-5p is upregulated in DRG ne

152 is critical for pain-like effects following nerve injury in mice, perhaps via a GPCR-mediated activa

153 Fifth lumbar (L5) nerve injury in rats causes neuropathic pain manifested

154 We found that nerve injury in rats induced a long-lasting reduction in

155 of cofilin activity is an acute response to nerve injury in the peripheral nervous system.

156 al root ganglia (DRGs) neurons after sciatic nerve injury in the rat.

157 derstand the mechanism of recovery following nerve injury in this species we investigated the process

158 tions and hastened recovery after peripheral nerve injury in wild type mice.

159 ion factor Sox11 as a key player after optic nerve injury-in DLK signaling of RGC cell death, and in

160 r the promotion of functional recovery after nerve injury.In vitroandin vivoanalysis of GSK3 single k

161 Nerve injury increased activity of euchromatic histone-l

162 Here, we report that peripheral nerve injury increases expression of the DNA methyltrans

163 A preconditioning nerve injury increases the levels of amphoterin protein

164 layed axon degeneration following peripheral nerve injury, indicating that it participates in the deg

165 We found that peripheral nerve injury induced de novo expression of colony-stimul

166 Unexpectedly, however, peripheral nerve injury induced significant GRP expression in a het

167 receptor 2 (TLR2) signaling is critical for nerve injury-induced activation of spinal cord microglia

168 This upregulation was responsible for nerve injury-induced de novo DNA methylation within the

169 Blocking this upregulation prevented nerve injury-induced DNA methylation within the promoter

170 Nerve injury-induced downregulation of voltage-gated pot

171 inct Panx1 inhibitors blocked development of nerve injury-induced hypersensitivity and partially reli

172 We showed here that blocking nerve injury-induced increase in G9a rescued Kcna2 mRNA

173 ing or blocking Schwann cell NOX1 attenuated nerve injury-induced macrophage infiltration, oxidative

174 s but inhibiting this pathway does not alter nerve injury-induced mechanical allodynia.

175 ical hypersensitivity, or in partial sciatic nerve injury-induced mechanical allodynia.

176 c pain, depletion of DRG macrophages reduces nerve injury-induced mechanical hypersensitivity and exp

177 neuron deletion of Csf1 completely prevented nerve injury-induced mechanical hypersensitivity and red

178 Blocking this increase prevents nerve injury-induced methylation of the voltage-dependen

179 actor 1 from sensory neurons, which prevents nerve injury-induced microglial activation and prolifera

180 evels are suppressed in the spinal cord in a nerve injury-induced neuropathic pain mouse model.

181 Although microglia have been implicated in nerve injury-induced neuropathic pain, the manner by whi

182 glion (DRG) neurons, which may contribute to nerve injury-induced neuropathic pain.

183 Spinal cord microglia contribute to nerve injury-induced neuropathic pain.

184 has a profound pain relieving effect against nerve injury-induced neuropathic pain.

185 or genetic knockdown of DRG DNMT1 alleviated nerve injury-induced pain hypersensitivities, DRG DNMT1

186 y in the injured DRG neurons, and alleviated nerve injury-induced pain hypersensitivities.

187 omized DRG and attenuated the development of nerve injury-induced pain hypersensitivity.

188 ics in the superficial dorsal horn; (2) that nerve injury-induced pain triggers changes in dendritic

189 gic epidermal nerve fibers in a rat model of nerve injury-induced pain.

190 mina II) neurons before and after peripheral nerve injury-induced pain.

191 or Ehmt2 knockout in DRG neurons normalized nerve injury-induced reduction in the inhibitory effect

192 ical inhibition of GT1b synthesis attenuates nerve injury-induced spinal cord microglia activation an

193 diated phosphorylation after SNL contributes nerve injury-induced tactile allodynia.SIGNIFICANCE STAT

194 Here, we show that nerve injury-induced upregulation of sialyltransferase S

195 of low-threshold mechanoreceptors (LTMRs) to nerve-injury-induced mechanical allodynia, we generated

196 ive spinal cord prevented the development of nerve-injury-induced mechanical hypersensitivity.

197 Nerve injury induces changes in gene transcription in do

198 Mechanistically, peripheral nerve injury induces DNA demethylation and upregulation

199 Peripheral nerve injury induces increased expression of thrombospon

200 As compared with inflammation, nerve injury induces much more robust morphologic activa

201 Interestingly, peripheral nerve injury induces tactile allodynia and upregulates C

202 Nerve injury inducing nociceptive hypersensitivity also

203 Following peripheral nerve injury, innocuous stimuli activated this nocicepti

204 on of dorsal horn microglia after peripheral nerve injury is a significant expansion and proliferatio

205 e whether, in humans, chronic pain following nerve injury is associated with altered ongoing function

206 Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in dam

207 Reinnervation timing after nerve injury is critical for favorable axonal regenerati

208 learance of axonal and myelin debris after a nerve injury is directed primarily by inflammatory CCR2(

209 Cranial nerve injury is disabling for patients, and facial nerve

210 lated inflammatory response after peripheral nerve injury is essential for axon regeneration and reco

211 injury is disabling for patients, and facial nerve injury is particularly debilitating due to combine

212 cold hypersensitivity induced by peripheral nerve injury is reduced in eIF4E(S209A) and Mnk1/2(-/-)

213 id proinflammatory response after peripheral nerve injury is required for clearance of tissue debris

214 Peripheral nerve injury leads to various injury-induced responses i

215 A-Seq data analyses indicate that peripheral nerve injury may result in highly selective mRNA enrichm

216 Conversely, in the absence of nerve injury, mimicking this increase reduces the Kcna2

217 ysis to investigate the relationship between nerve injury, mitochondrial localization, and axon regen

218 ted hypersensitivity generated by the spared nerve injury model of neuropathic pain was reversed by i

219 In the rodent nerve injury model of neuropathic pain, BDNF-mediated lo

220 allodynia in a chronic, neuropathic sciatic nerve injury model, but tolerance to morphine developed

221 erent microglia phenotypes in a murine optic nerve injury model.

222 te Freund's adjuvant) or neuropathic (spared nerve injury) model of persistent pain, we observed that

223 l and thermal hypersensitivity in peripheral nerve injury models of neuropathic pain.

224 ns (NAc) neurons in mouse and rat peripheral nerve injury models of neuropathic pain.

225 otected from hypersensitivity in two sciatic nerve injury models.

226 chronic constriction injury (CCI) and spared nerve injury models.

227 While a regeneration-competent peripheral nerve injury mounts a regenerative gene expression respo

228 here is consensus that, distal to peripheral nerve injury, myelin and Remak cells reorganize to form

229 regulated by myelinating Schwann cells after nerve injury, myelin debris was present in autophagosome

230 of regeneration associated genes upon optic nerve injury nor the increased regenerative potential of

231 McKeown RAMIE procedure, recurrent laryngeal nerve injury occurred in 3% and 11% of patients, respect

232 Two nerve injuries of the superficial peroneal nerve were re

233 nerve might mimic the stimulatory effect of nerve injury on the regenerative state of the primary se

234 nder pathophysiological conditions following nerve injury or diabetic neuropathy, the slightest touch

235 derate to severe chronic pain resulting from nerve injury or disorder, affects 6.9%-10% of the global

236 roup developed permanent recurrent laryngeal nerve injury or hyperparathyroidism.

237 namic mechanical hypersensitivity induced by nerve injury or inflammation in mice by ablating a group

238 ming of the Schwann cell transcriptome after nerve injury, our results have highlighted a novel epige

239 ry vein damage (P = 0.864) and long thoracic nerve injury (P = 0.094).

240 erapies to reduce painful recovery times for nerve-injury patients, by accelerating the rate at which

241 h spared nerve injury, a model of peripheral nerve injury (PNI)-induced neuropathic pain.

242 Neuropathic pain caused by nerve injury presents with severe spontaneous pain and a

243 dent pathway activated by TSP4 or peripheral nerve injury promotes exaggerated presynaptic excitatory

244 median follow-up, including: stroke, phrenic nerve injury, PV stenosis, and esophageal injury.

245 ntly, diagnosis and monitoring of peripheral nerve injury relies on clinical and electrodiagnostic in

246 Iatrogenic nerve injury remains a significant cause of morbidity in

247 reconstructive surgery) from other types of nerve injury remains unknown.

248 In mice, spared nerve injury replicates symptoms of human neuropathic pa

249 These findings reveal a role of the nerve injury response, particularly through functions of

250 chwann cells, resulting in activation of the nerve injury response.

251 ndings explain how DLK specifically mediates nerve injury responses and reveal a novel cellular mecha

252 Peripheral nerve injury results in persistent motor deficits, even

253 active at the end target muscle after motor nerve injury reveals new therapeutic targets that may tr

254 ld-type mice, following transient peripheral nerve injury, reversed the overexpression of genes in mu

255 After nerve injury, Schwann cells convert to a phenotype speci

256 alterations in Ia-circuit function following nerve injuries.SIGNIFICANCE STATEMENT Synaptic plasticit

257 rvation and functional muscle recovery after nerve injury.SIGNIFICANCE STATEMENT This work demonstrat

258 Neuropathic pain caused by peripheral nerve injuries significantly affects sensory perception

259 ) and CCR2(+) monocytes infiltrate the optic nerve injury site and remain present for months.

260 ion of DRG macrophages, but not those at the nerve injury site, to both the initiation and maintenanc

261 itment occurred at the NMJ, distant from the nerve injury site, to support functional recovery at the

262 /DU, outbred: Crl:SD) were exposed to Spared Nerve Injury (SNI) and evaluated routinely for 6 months

263 The spared nerve injury (SNI) model of neuropathic pain increases P

264 In the spared nerve injury (SNI) model of neuropathic pain, NPY-sapori

265 nisms of mPFC deactivation in the rat spared nerve injury (SNI) model of neuropathic pain.

266 to define their gene profiling in rat spared nerve injury (SNI) model of neuropathic pain.

267 reversed tactile allodynia in a mouse spared-nerve injury (SNI) model.

268 elopment of SC lineage and during peripheral nerve injury, so we sought to study their functional pro

269 It was shown that nerve injury strengthens synaptic input from the BLA ont

270 namic mechanical hypersensitivity induced by nerve injury, suggesting that these neurons may be a cel

271 milar transcriptional response to peripheral nerve injury that both promotes axonal regeneration and

272 se a series of neural and glial events after nerve injury that result in the generation of altered th

273 However, in a significant proportion of nerve injuries, the likelihood of spontaneous regenerati

274 Within hours of a sciatic nerve injury, the level of phosphorylated cofilin dramat

275 e transplants were performed before or after nerve injury, the MGE cells developed into mature neuron

276 In response to nerve injury, the two resident snMac populations respond

277 tal stimulators in a rat model of peripheral nerve injuries, thereby demonstrating the potential of p

278 1 did not develop neuropathic pain following nerve injury, thereby identifying astrocytes as the prim

279 sufficient to recover hypersensitivity after nerve injury; this rescue required expression of a Panx1

280 sensory neurons regenerate their axon after nerve injury to enable functional recovery.

281 localize treatments for neuropathic pain and nerve injury to injured nerves.

282 ind that DLK-activating insults ranging from nerve injury to neurotrophin deprivation result in both

283 l root ganglion neurons following peripheral nerve injury, triggering selective degeneration of injur

284 toantigenic peptide endogenously released in nerve injury triggers multisite, sex-specific transcript

285 endent anion channel 1 (VDAC1) after sciatic nerve injury triggers Schwann cell demyelination via ERK

286 Nerve injury triggers the conversion of myelin and non-m

287 After nerve injury, tSCs extend cytoplasmic processes between

288 Finally, nerve injury upregulated CXCL12 in lumbar L4-L6 DRGs, an

289 Peripheral nerve injury upregulated DNMT1 expression in the injured

290 The role of IL-10 in nerve injury was assessed using IL-10-null mice.

291 In addition to Wallerian degeneration, nerve injury was significantly aggravated (P = 0.032) af

292 rotein (MBP(84-104)) fragment released after nerve injury, we demonstrate that exposing the sciatic n

293 Finally, in an animal model of optic nerve injury, we observed early glial activation and dem

294 ing paradigms of peripheral inflammation and nerve injury, we show that the prevention of RGS4 action

295 All nerve injuries were recorded.

296 elination and target reinnervation following nerve injury, which resulted in slowed recovery of motor

297 hat light-evoked behaviors were unchanged by nerve injury, which suggests that activation of Vglut1-p

298 lated in the dorsal root ganglia (DRG) after nerve injury, which was further validated for its mouse

299 n ultrasonic, broadband clicks after sciatic nerve injury, which was reversed by THC, CBD, and morphi

300 t-mTORC1 signaling in the muscle response to nerve injury, with important implications for neuromuscu