Relationship between sprouting axons, proteoglycans and glial cells following unilateral nigrostriatal axotomy in the adult rat

Moon, Lawrence; Asher, RA; Rhodes, KE; Fawcett, James W.

doi:10.1016/s0306-4522(01)00457-2

Cited by 91 publications

(67 citation statements)

References 94 publications

(103 reference statements)

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“…Miyake et al, 1988;Mitchell et al, 1993;Di Prospero et al, 1998), infusion of the antimitotic did not appear to influence their injury response. The presence of astrocytes probably contributed to the limited ability of axons to re- The non-infused animals showed a greater up-regulation of GFAP cells than infused animals, particularly close to the lesion borders, suggesting that the region of scar tissue surrounding the lesion is slightly modified by the infusion (consistent with previous findings from our laboratory; Moon et al, 2002).…”

Section: Astrocytessupporting

confidence: 89%

Inhibiting cell proliferation during formation of the glial scar: effects on axon regeneration in the CNS

2003

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Abstract-Following a CNS lesion many glial cell types proliferate and/or migrate to the lesion site, forming the glial scar. The majority of these cells express chondroitin sulphate proteoglycans (CS-PGs), previously shown to inhibit axonal growth. In this study, in an attempt to diminish glial scar formation and improve axonal regeneration, proliferating cells were eliminated from the lesion site. Adult rats received a continuous infusion of 2% cytosine-D-arabinofuranoside (araC) or saline for 7 days over the lesion site, immediately following a unilateral transection of the right medial forebrain bundle. Additional groups of rats that received subdural infusions prior to the lesion, and lesioned rats which received no infusion, were also compared in the analyses. Animals were killed at 4, 7, 12 or 18 days postlesion (dpl) and immunohistochemistry was used to determine the effects of these treatments on tyrosine hydroxylase (TH)-lesioned axons, and on the injury response of glial cells. Almost complete elimination of NG2 oligodendrocyte progenitor cells from the lesion site was seen up to 7 dpl in araCinfused animals; reduced numbers of reactive CD11b microglia were also seen but no effects were seen on the injury response of GFAP astrocytes. Significantly more TH axons were seen distal to the lesion in araC-treated brains, but these numbers dwindled by 18 dpl.

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Section: Astrocytessupporting

confidence: 89%

Inhibiting cell proliferation during formation of the glial scar: effects on axon regeneration in the CNS

2003

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“…range of CNS injuries 21,71,72 . Importantly, pre-critical period embryonic reactive astroglia do not upregulate CSPGs after injury 73,74 …”

Section: Dorsal Root Ganglionmentioning

confidence: 99%

Regeneration beyond the glial scar

2004

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“…4,12,22,28,49 The neu rons in the CNS have a limited capacity to regenerate after an injury in contrast to the peripheral nervous system. 29 However, it was recognized more than two decades ago that CNS axons can regenerate when provided with a permissive environment.…”

Section: 13mentioning

confidence: 99%

Suppression of neurocan and enhancement of axonal density in rats after treatment of traumatic brain injury with scaffolds impregnated with bone marrow stromal cells

Mahmood¹,

Wu²,

Qu³

et al. 2014

JNS

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Bone marrow stromal cells (MSCs) are a heterogeneous subpopulation of bone marrow cells that includes mesenchymal stem and progenitor cells. Extensive research conducted during the last decade has shown great promise for MSCs as an effective therapy for traumatic brain injury (TBI) in experimental models 32-35, 37-41,52 and potentially in clinical settings. Also the underlying mechanisms of action of MSCs have been demonstrated to be neuro-restorative rather than neuro-substitutive. 33 Among their neural remodeling effects, MSCs have been shown to promote axonal sprouting in the brain and spinal cord. 42,60 The present study focuses on the ability of MSCs to inhibit neurocan, one of the growth-inhibitory molecules (growth-IMs) that suppress axonal regeneration after neural injury. 18,25 The molecular mechanisms involved in axonal regeneration after neural injury are still unclear; however, over the last few years growth-IMs that have a repulsive effect Suppression of neurocan and enhancement of axonal density in rats after treatment of traumatic brain injury with scaffolds impregnated with bone marrow stromal cells Object. Neurocan is a major form of growth-inhibitory molecule (growth-IM) that suppresses axonal regeneration after neural injury. Bone marrow stromal cells (MSCs) have been shown to inhibit neurocan expression in vitro and in animal models of cerebral ischemia. Therefore, the present study was designed to investigate the effects of treatment of MSCs impregnated with collagen scaffolds on neurocan expression after traumatic brain injury (TBI).Methods. Adult male Wistar rats were injured with controlled cortical impact and treated with saline, human MSCs (hMSCs) (3 × 10 6 ) alone, or hMSCs (3 × 10 6 ) impregnated into collagen scaffolds (scaffold + hMSCs) transplanted into the lesion cavity 7 days after TBI (20 rats per group). Rats were sacrificed 14 days after TBI, and brain tissues were harvested for immunohistochemical studies, Western blot analyses, laser capture microdissections, and quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) to evaluate neurocan protein and gene expressions after various treatments.Results. Animals treated with scaffold + hMSCs after TBI showed increased axonal and synaptic densities compared with the other groups. Scaffold + hMSC treatment was associated with reduced TBI-induced neurocan protein expression and upregulated growth-associated protein 43 (GAP-43) and synaptophysin expression in the lesion boundary zone. In addition, animals in the scaffold + hMSC group had decreased neurocan transcription in reactive astrocytes after TBI. Reduction of neurocan expression was significantly greater in the scaffold + hMSC group than in the group treated with hMSCs alone.Conclusions. The results of this study show that transplanting hMSCs with scaffolds enhances the effect of hMSCs on axonal plasticity in TBI rats. This enhanced axonal plasticity may partially be attributed to the downregulation of neurocan expression by hMSC treatment after in...

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Relationship between sprouting axons, proteoglycans and glial cells following unilateral nigrostriatal axotomy in the adult rat

Cited by 91 publications

References 94 publications

Inhibiting cell proliferation during formation of the glial scar: effects on axon regeneration in the CNS

Inhibiting cell proliferation during formation of the glial scar: effects on axon regeneration in the CNS

Regeneration beyond the glial scar

Suppression of neurocan and enhancement of axonal density in rats after treatment of traumatic brain injury with scaffolds impregnated with bone marrow stromal cells

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