ライフサイエンスコーパス: glial scar

1 not be the main CSPG contributory factor in glial scar.

2 lycans participating in the formation of the glial scar.

3 itory signals associated with myelin and the glial scar.

4 to the inhibitors associated with myelin and glial scar.

5 CSPGs), the major class of inhibitors in the glial scar.

6 ycans, the major inhibitory molecules in the glial scar.

7 n the pia mater but not in astrocytes in the glial scar.

8 tes become reactive and in many cases form a glial scar.

9 cluding the formation and maintenance of the glial scar.

10 nd versican are not expressed in the chronic glial scar.

11 pregulated by the reactive astrocytes at the glial scar.

12 restricted to the reactive astrocytes at the glial scar.

13 otentially related to the attenuation of the glial scar.

14 l lobe epilepsy hinges on the removal of the glial scar.

15 rograms and an inhibitory environment from a glial scar.

16 ate in large numbers among astrocytes in the glial scar.

17 al changes resulting in the formation of the glial scar.

18 t dendrite and the formation of a persistent glial scar.

19 or how single astrocytes combine to form the glial scar.

20 c axons in the inhibitory environment of the glial scar.

21 tory proteins associated with myelin and the glial scar.

22 dystrophic axons in an in vitro model of the glial scar.

23 avities, as well as the number of subretinal glial scars.

24 iated proteins and proteoglycans enriched in glial scars.

25 ry injury processes as well as in diminished glial scarring.

26 d in chronic phase may be due to preexisting glial scarring.

27 lect continuous axons and may instead depict glial scarring.

28 th, while its appearance on glia may promote glial scarring.

29 n of AQP4 expression or function might alter glial scarring.

30 with the NG2 CSPG, a major component of the glial scar, activates PKCzeta, and this activation is bo

31 e mechanisms underlying the formation of the glial scar after injury are poorly understood.

32 vivo model of reactive gliosis: that is, the glial scar, after cortical injury.

33 -6 could participate in the formation of the glial scar and confer anti-inflammatory properties.

34 s integral to the formation of an inhibitory glial scar and cytoskeleton-mediated astrocyte migration

35 mice expressing MMPs developed a more severe glial scar and enhanced expression of chondroitin sulfat

36 l contusion site with ChABC treatment of the glial scar and glial cell line-derived neurotrophic fact

37 sulted in sensory axon regeneration past the glial scar and into the white matter rostral to the inju

38 in sulphate proteoglycans (CSPGs) within the glial scar and perineuronal net creates a barrier to axo

39 of the tumor with the presence of a residual glial scar and reactive changes, mainly presence of hemo

40 scades that result in the development of the glial scar and the exclusion of meningeal fibroblasts fr

41 ation results in the formation of the neural/glial scar and the reconstitution of the glial limitans.

42 fter injury by regulating the formation of a glial scar and white matter sparing and/or axonal plasti

43 he peak of acute disease (day 14), prevented glial scarring and ameliorated the disease severity.

44 We also conclude that in the absence of glial scarring and irreversible neuronal injury, in vivo

45 Glial scarring and outer limiting membrane integrity, fe

46 ng and axonal plasticity, the formation of a glial scar, and locomotor recovery after spinal cord inj

47 egeneration, attenuates the formation of the glial scar, and significantly enhances functional recove

48 More than half of the astrocytes in the glial scar are generated by ependymal cells, the neural

49 sic neuronal programs and the formation of a glial scar are the main obstacles.

50 e signals that initiate the formation of the glial scar are unknown.

51 lized fibrotic scar surrounded by a reactive glial scar at the lesion site.

52 droitin sulfate proteoglycans (CSPG), in the glial scar at the lesion; and (2) the diminished growth

53 physical or molecular barriers presented by glial scarring at the lesion site, it has been suggested

54 NT-3 can achieve axonal bridging beyond the glial scar, but growth for longer distances is not susta

55 levated, indicating that modification of the glial scar by ChABC promotes long-lasting signaling chan

56 egeneration of adult axons in the absence of glial scarring, by using a microtransplantation techniqu

57 lt myelinated white matter tracts beyond the glial scar can be highly permissive for regeneration.

58 osphacan protein levels are decreased in the glial scar compared with the uninjured brain.

59 The resulting glial scar consists of an irregular array of astrocyte p

60 At sites of CNS injury, a glial scar develops, containing extracellular matrix mol

61 , and enzymatically modulated the inhibitory glial scar distal to the graft.

62 ctive, we discuss the divergent roles of the glial scar during CNS regeneration and explore the possi

63 be a promising therapeutic target to reduce glial scarring during wound healing after spinal cord in

64 s in the sequence of events that can lead to glial scarring, edema, seizure and neuronal death.

65 as well as the inhibitory environment of the glial scar established around the lesion site.

66 esive interactions between astrocytes at the glial scar, even though reactive gliosis and scar format

67 s a key role in astrogliosis associated with glial scar formation after brain injury.

68 s in cellular responses resulted in abnormal glial scar formation after injury, and significantly inc

69 n deleterious effects of BMPR1b signaling on glial scar formation after SCI.

70 is necessary for neuroprotection and normal glial scar formation after SCI.

71 ith neuronal and oligodendroglial apoptosis, glial scar formation and microglial activation.

72 the nuclear pore complex (NPC) required for glial scar formation and reduced gamma oscillations in m

73 Although astrocytes participate in glial scar formation and tissue repair, dysregulation of

74 s demonstrate that it is possible to inhibit glial scar formation and to facilitate regeneration afte

75 Glial scar formation around implanted silicon neural pro

76 nd tissue is suspected to be a key driver of glial scar formation around neural implants.

77 This contributes to glial scar formation at the lesion border and gliosis in

78 bility of soft hydrogel coatings to modulate glial scar formation by reducing local strain.

79 egulation may enable targeted suppression of glial scar formation in diverse neurological disorders.

80 abolishes the fibrinogen-induced effects on glial scar formation in vivo and in vitro.

81 ary and secondary axotomy, inflammation, and glial scar formation that have devastating effects on ne

82 rves as an early signal for the induction of glial scar formation via the TGF-beta/Smad signaling pat

83 cytokines leads to dramatic inflammation and glial scar formation, affecting brain tissue's ability t

84 ating lesion causes upregulation of gliosis, glial scar formation, and heightened expression of CSPGs

85 ive suppressor of Muller cell proliferation, glial scar formation, and photoreceptor cell death in a

86 ions in the CNS, including the initiation of glial scar formation, angiogenesis, and maintenance of t

87 ding to cell death, axonal degeneration, and glial scar formation, exacerbating the already hostile e

88 In brain, AQP4 facilitates water balance and glial scar formation, which are important determinants o

89 Spinal cord injury is followed by glial scar formation, which has positive and negative ef

90 SCI) leads to irreversible neuronal loss and glial scar formation, which ultimately result in persist

91 the response of astrocytes to injury and in glial scar formation.

92 for astrocyte hyperplasia, hypertrophy, and glial scar formation.

93 thus may serve as a novel target to control glial scar formation.

94 the initial molecular mediator that triggers glial scar formation.

95 erotonin-immunoreactive fibers traversed the glial scars formed at both cord-graft interfaces.

96 In the injured spinal cord, a glial scar forms and becomes a major obstacle to axonal

97 surprising inability to regenerate even in a glial scar-free environment.

98 nd that degenerating white matter beyond the glial scar has a far greater intrinsic ability to suppor

99 on regeneration, beneficial functions of the glial scar have also been recently identified.

100 n lesions after ablation formed a persistent glial scar in 5 (31.3%) patients.

101 le reducing the inhibitory properties of the glial scar in axon regeneration.

102 We have successfully removed an existing glial scar in chronically contused rat spinal cord using

103 his level may facilitate manipulation of the glial scar in inflammatory disorders of the human CNS.

104 so, BMPR1b knock-out mice have an attenuated glial scar in the chronic stages following injury, sugge

105 y tissue damage, progressive cavitation, and glial scarring in the CNS.

106 l detachment, Muller cells formed subretinal glial scars in the wt mice.

107 lfate proteoglycans (CSPGs) found within the glial scar inhibit axon regeneration but the intracellul

108 Formation of the glial scar involves migration of astrocytes toward the l

109 he subacute and chronic phases of injury the glial scar is a physical and biochemical barrier to axon

110 Glial scar is a significant barrier to neural implant fu

111 nt in astrocyte migration and formation of a glial scar is unknown.

112 migratory potential and ability to penetrate glial scars is higher.

113 One such response, the glial scar, is a structural formation of reactive glia a

114 ory molecules associated with myelin and the glial scar limit axon regeneration in the adult central

115 mical constraints imposed by the periinfarct glial scar may contribute to the limited clinical improv

116 pletion of adult OPCs, inhibition within the glial scar, or damage to the axons that prevents myelina

117 hrough white matter tracts, gray matter, and glial scars, overcoming the inhibitory nature of the CNS

118 and the TSG-6 protein is present within the glial scar, potentially coordinating and stabilizing the

119 Whereas glial scarring presents a roadblock for mammalian spinal

120 -21 in regulating astrocytic hypertrophy and glial scar progression after SCI, and suggest miR-21 as

121 ry, suggesting that it has a greater role in glial scar progression.

122 Glial scar reformation was effectively prevented after a

123 omoting a permissive microenvironment in the glial scar region.

124 late in chronic phase (day 78), significant glial scarring remained and the clinical severity did no

125 glia largely segregate into the fibrotic and glial scars, respectively; therefore, we used a thymidin

126 an expression increases significantly in the glial scar resulting from cortical injury, including the

127 tional heterogeneity within the cells of the glial scar-specifically, astrocytes, NG2 glia and microg

128 Mammalian glial scars supposedly form a chemical and mechanical ba

129 glycans (CSPGs) are a major component of the glial scar that contributes to the limited regeneration

130 hey migrate, undergo hypertrophy, and form a glial scar that inhibits axon regeneration.

131 We now have an in vitro model of the glial scar that may serve as a potent tool for developin

132 have developed a novel in vitro model of the glial scar that mimics the gradient of proteoglycan foun

133 Glial scars that form at CNS injury sites block axon reg

134 Levels of NG2 increase rapidly in the glial scars that form at sites of CNS injury, suggesting

135 Strikingly, after crossing the distal glial scar, these fibers elongated in white and periaque

136 ajor axon growth inhibitory component of the glial scar tissue that blocks successful regeneration.

137 ognizes tenascin-C, one of the components of glial scar tissue, and an integrin activator.

138 atly enlarged secondary injury surrounded by glial scar tissue, is a poorly understood complication o

139 of CSPGs are highly upregulated by reactive glial scar tissues after injuries and form a strong barr

140 ganglion neurons in an in vitro model of the glial scar to examine macrophage-axon interactions and o

141 m cells were also more efficient in reducing glial scar volume and expression of chondroitin sulfates

142 The glial scar was also altered in the absence of acutely di

143 Also, demyelination and glial scarring were significantly decreased in MMPI-trea

144 ar composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged a

145 ns are the principal inhibitory component of glial scars, which form after damage to the adult centra

146 creased CSPG deposition and development of a glial scar, while also increasing axon growth after spin

147 We also hypothesized that treating the glial scar with chondroitinase ABC (ChABC), which digest

148 rimary contributors to the growth-inhibitory glial scar, yet they are also neuroprotective and can fo