Optic nerve regeneration in polyglycolic acid–chitosan conduits coated with recombinant L1-Fc

Xu, Gang; Nie, Duyu; Wen-zu, Wang; Zhang, Peihua; Shen, Jie; Ang, Beng-Ti; Li, Guohua; Luo, Xi; Chen, Nan-liang; Xiao, Zhicheng

doi:10.1097/00001756-200410050-00004

Cited by 51 publications

(47 citation statements)

References 22 publications

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“…The adhesion molecule L1 favors axonal growth in an inhibitory environment (Castellani et al, 2002;Dong et al, 2002;Fransen et al, 1998;Lemmon et al, 1989;Roonprapunt et al, 2003;Xu et al, 2004;Zhang et al, 2005), promotes neurite outgrowth, and displays survival-promoting effects on cultured central nervous system neurons (Chen et al, 1999;Dong et al, 2002;Dong et al, 2003;Lemmon et al, 1989;Lindner et al, 1983;Rathjen and Rutishauser, 1984). We found that T4as-NPCs overexpress L1 and survive better in the lesioned area, suggesting that L1 positively influences NPC survival, even after grafting into a hostile environment.…”

Section: Discussionmentioning

confidence: 68%

“…In particular, it has been proposed that T4 exerts its neuropromoting effects, at least partly, via mechanisms that involve activation of the cell adhesion molecule Journal of Cell Science 122 (22) L1. The neuronal recognition molecule L1 has been shown to favor axonal growth in an inhibitory environment (Castellani et al, 2002;Chen et al, 2007;Roonprapunt et al, 2003;Xu et al, 2004;Zhang et al, 2005). On the basis of these observations, we investigated whether the functional improvement of mice transplanted with T4as-NPCs might be due to increased L1 expression.…”

Section: Transplanted T4as-npcs Survive and Differentiate In Injuredmentioning

confidence: 99%

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Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Mollinari

Ricci–Vitiani

Pieri

et al. 2009

Journal of Cell Science

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Thymosin β4 (Tβ4) is an actin-binding peptide whose expression in developing brain correlates with migration and neurite extension of neurons. Here, we studied the effects of the downregulation of Tβ4 expression on growth and differentiation of murine neural progenitor cells (NPCs), using an antisense lentiviral vector. In differentiation-promoting medium, we found twice the number of neurons derived from the Tβ4-antisense-transduced NPCs, which showed enhanced neurite outgrowth accompanied by increased expression of the adhesion complex N-cadherin–β-catenin and increased ERK activation. Importantly, when the Tβ4-antisense-transduced NPCs were transplanted in vivo into a mouse model of spinal cord injury, they promoted a significantly greater functional recovery. Locomotory recovery correlated with increased expression of the regeneration-promoting cell adhesion molecule L1 by the grafted Tβ4-antisense-transduced NPCs. This resulted in an increased number of regenerating axons and in sprouting of serotonergic fibers surrounding and contacting the Tβ4-antisense-transduced NPCs grafted into the lesion site. In conclusion, our data identify a new role for Tβ4 in neuronal differentiation of NPCs by regulating fate determination and process outgrowth. Moreover, NPCs with reduced Tβ4 levels generate an L1-enriched environment in the lesioned spinal cord that favors growth and sprouting of spared host axons and enhances the endogenous tissue-repair processes.

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Section: Discussionmentioning

confidence: 68%

Section: Transplanted T4as-npcs Survive and Differentiate In Injuredmentioning

confidence: 99%

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Mollinari

Ricci–Vitiani

Pieri

et al. 2009

Journal of Cell Science

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“…it is downregulated on myelinated axons and re-expressed in regenerating axons after spinal cord injury [64,65] . Exogenous L1CAM is beneficial in promoting axon growth and functional recovery after spinal cord injury [66] and optic nerve lesion [67] and is involved in the regenerative growth of Purkinje cell axons in vivo [68] .…”

Section: Cell Adhesion Moleculesmentioning

confidence: 99%

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Zhang

Guo

2013

Neurosci. Bull.

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Multiple sclerosis (MS) is a chronic and devastating autoimmune demyelinating disease of the central nervous system. With the increased understanding of the pathophysiology of this disease in the past two decades, many disease-modifying therapies that primarily target adaptive immunity have been shown to prevent exacerbations and new lesions in patients with relapsing-remitting MS. However, these therapies only have limited efficacy on the progression of disability. Increasing evidence has pointed to innate immunity, axonal damage and neuronal loss as important contributors to disease progression. Remyelination of denuded axons is considered an effective way to protect neurons from damage and to restore neuronal function. The identification of several key molecules and pathways controlling the differentiation of oligodendrocyte progenitor cells and myelination has yielded clues for the development of drug candidates that directly target remyelination and neuroprotection. The long-term efficacy of this strategy remains to be evaluated in clinical trials. Here, we provide an overview of current and emerging therapeutic concepts, with a focus on the opportunities and challenges for the remyelination approach to the treatment of MS.

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“…We have shown previously that L1 influences differentiation of neural stem cells into neurons in vitro (Dihné et al, 2003). Furthermore, L1 has been shown to promote functional recovery in adult rats after contusion-induced spinal cord injury (Roonprapunt et al, 2003) and optic nerve lesion (Xu et al, 2004) and is involved in regenerative growth of Purkinje cell axons in vivo (Zhang et al, 2005), thus overcoming regeneration-adversive cues that prevail in the CNS of adult mammals.…”

Section: Introductionmentioning

confidence: 99%

Neural Cell Adhesion Molecule L1-Transfected Embryonic Stem Cells Promote Functional Recovery after Excitotoxic Lesion of the Mouse Striatum

Bernreuther¹,

Dihné²,

Johann³

et al. 2006

J. Neurosci.

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We have generated a murine embryonic stem cell line constitutively expressing L1 at all stages of neural differentiation to investigate the effects of L1 overexpression on stem cell proliferation, migration, differentiation, cell death, and ability to influence drug-induced rotation behavior in an animal model of Huntington's disease. L1-transfected cells showed decreased cell proliferation in vitro, enhanced neuronal differentiation in vitro and in vivo, and decreased astrocytic differentiation in vivo without influencing cell death compared with nontransfected cells. L1 overexpression also resulted in an increased yield of GABAergic neurons and enhanced migration of embryonic stem cell-derived neural precursor cells into the lesioned striatum. Mice grafted with L1-transfected cells showed recovery in rotation behavior 1 and 4 weeks, but not 8 weeks, after transplantation compared with mice that had received nontransfected cells, thus demonstrating for the first time that a recognition molecule is capable of improving functional recovery during the initial phase in a syngeneic transplantation paradigm.

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Optic nerve regeneration in polyglycolic acid–chitosan conduits coated with recombinant L1-Fc

Cited by 51 publications

References 22 publications

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Promoting remyelination for the treatment of multiple sclerosis: opportunities and challenges

Neural Cell Adhesion Molecule L1-Transfected Embryonic Stem Cells Promote Functional Recovery after Excitotoxic Lesion of the Mouse Striatum

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