Evidences that β1 integrin and Rac1 are involved in the overriding effect of laminin on myelin-associated glycoprotein inhibitory activity on neuronal cells

Laforest, Sullivan; Milanini, Julie; Parat, Fabrice; Thimonier, Jean; Lehmann, Maxime

doi:10.1016/j.mcn.2005.08.006

Cited by 13 publications

(16 citation statements)

References 55 publications

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“…1A). These results are consistent with earlier studies showing that signaling events activated by laminin can abolish the inhibitory effect of CNS myelins (David et al, 1995), and a more recent study that laminin overrides the inhibitory effect of MAG (Laforest et al, 2005). In significant contrast, aggrecan, a component of CSPGs, significantly abolished NGF-induced axon assembly of naive neurons cultured in the presence of laminin (Fig.…”

Section: Resultssupporting

confidence: 93%

“…Indeed, a previous observation has shown that laminin is able to overcome the inhibitory effect of CNS myelins (David et al, 1995). Moreover, a recent study has also demonstrated that laminin is able to override the inhibitory effect of MAG by regulation of Rac activity (Laforest et al, 2005). By contrast, aggrecan significantly blocked axon assembly under the same experimental conditions.…”

Section: Discussionmentioning

confidence: 92%

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Neurotrophins support regenerative axon assembly over CSPGs by an ECM-integrin-independent mechanism

Zhou

Walzer

et al. 2006

Journal of Cell Science

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Chondroitin sulfate proteoglycans (CSPGs) and myelin-based inhibitors are the most studied inhibitory molecules in the adult central nervous system. Unlike myelin-based inhibitors, few studies have reported ways to overcome the inhibitory effect of CSPGs. Here, by using regenerating adult dorsal root ganglion (DRG) neurons, we show that chondroitin sulfate proteoglycans inhibit axon assembly by a different mechanism from myelin-based inhibitors. Furthermore, we show that neither Rho inhibition nor cAMP elevation rescues extracellular factor-induced axon assembly inhibited by CSPGs. Instead, our data suggest that CSPGs block axon assembly by interfering with integrin signaling. Surprisingly, we find that nerve growth factor (NGF) promotes robust axon growth of regenerating DRG neurons over CSPGs. We have found that, unlike naive neurons that require simultaneous activation of neurotrophin and integrin pathways for axon assembly, either neurotrophin or integrin signaling alone is sufficient to induce axon assembly of regenerating neurons. Thus, our results suggest that the ability of NGF to overcome CSPG inhibition in regenerating neurons is probably due to the ability of regenerating neurons to assemble axons using an integrin-independent pathway. Finally, our data show that the GSK-3β-APC pathway, previously shown to mediate developing axon growth, is also necessary for axon regeneration.

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Section: Resultssupporting

confidence: 93%

Section: Discussionmentioning

confidence: 92%

Neurotrophins support regenerative axon assembly over CSPGs by an ECM-integrin-independent mechanism

Zhou

Walzer

et al. 2006

Journal of Cell Science

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“…EphA expression), as higher concentrations of ephrin-A5 stall axon outgrowth by temporal RGC axons on LN (Woo et al, 2009). LN also blocks the inhibitory effects of myelin-associated glycoprotein (MAG) (David et al, 1995; Laforest et al, 2005), which is responsible in part for limited regeneration by adult mammalian CNS neurons after injury (Cafferty et al, 2010). These observations have important implications for axonal regeneration in the adult mammalian CNS.…”

Section: Ecm Composition and Functionmentioning

confidence: 99%

Regulation of axonal outgrowth and pathfinding by integrin–ecm interactions

Myers

Santiago-Medina

Gómez

2011

Developmental Neurobiology

191

186

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Developing neurons use a combination of guidance cues to assemble a functional neural network. A variety of proteins immobilized within the extracellular matrix (ECM) provide specific binding sites for integrin receptors on neurons. Integrin receptors on growth cones associate with a number of cytosolic adaptor and signaling proteins that regulate cytoskeletal dynamics and cell adhesion. Recent evidence suggests that soluble growth factors and classic axon guidance cues may direct axon pathfinding by controlling integrin-based adhesion. Moreover, since classic axon guidance cues themselves are immobilized within the ECM and integrins modulate cellular responses to many axon guidance cues, interactions between activated receptors modulate cell signals and adhesion. Ultimately, growth cones control axon outgrowth and pathfinding behaviors by integrating distinct biochemical signals to promote the proper assembly of the nervous system. In this review, we discuss our current understanding how ECM proteins and their associated integrin receptors control neural network formation.

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“…Peripheral axons were shown to regenerate on laminin matrix in acellular grafts of sciatic nerve (Krekoski et al, 2001). Several intracellular signaling pathways are known to mediate the positive effects of NTFs and laminin on axonal growth (Laforest et al, 2005;Liu et al, 2002;Liu and Snider, 2001;Markus et al, 2002;Paglini et al, 1998;, but the integral behavior of the signaling network converting receptor activation into axonal growth remains largely unknown (Tucker et al, 2005). Importantly, co-signaling by soluble NTFs and substrate-bound ECM molecules integrates two significantly different types of intercellular communication: long-range messages from remotely diffusing messengers and those that are highly localized to matrix.…”

Section: Introductionmentioning

confidence: 99%

Neurotrophic factors switch between two signaling pathways that trigger axonal growth

Paveliev

Lume

Velthut

et al. 2007

Journal of Cell Science

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There is a major unsolved question in modern cell biology: how does a cell convey environmental information (receptor inputs) into adaptive behavioral programs (motility, gene expression, etc.) (Bray, 1995). A single cell has hundreds of different types of receptor proteins on its surface, making complex combinatorial relationships possible between signaling inputs and signaling network behavior. It remains largely unclear how different combinations of receptor signaling inputs are differentially recognized by the signaling network in such a way as to trigger execution of particular cellular events, such as gene transcription or cytoskeletal rearrangement. Signaling pathways downstream of different receptors are known to crosstalk at many levels and to converge at a limited number of signaling targets. A complex network of signaling pathways mediates the regulatory effects of neurotrophic factors (NTFs) and extracellular matrix (ECM) molecules on a wide spectrum of processes in neurons, including synaptic transmission, axonal growth and posttraumatic regeneration. Many signaling elements of those pathways have been characterized and activatory or inhibitory effects of particular elements on cell function have been described. At the same time, the integral functioning of the signaling network is just beginning to be addressed. It remains largely unclear how distinct pathways are orchestrated in the integrated network to produce highly specific cell responses to receptor stimulation.A critical obstacle to progress in our understanding of cell signaling networks is the lack of a standard unambiguous language allowing quantitative description and analysis of the network behavior (Lazebnik, 2002). The formalism of Boolean algebra was previously used to analyze a genetic network in the specific case of the bacteriophage lambda lysis-lysogeny decision (McAdams and Shapiro, 1995) and it was theoretically predicted that protein kinase signaling networks can be described in Boolean terms (Bhalla, 2003;Bray, 1995;Huang and Ingber, 2000). Moreover, signaling molecules with particular gating behaviors have been generated by means of protein domain recombination (Dueber et al., 2003;Dueber et al., 2004). In the present work, we considered a Boolean network formalism as a framework for experimental design and the interpretation of experimental data on a signaling network behavior.ECM molecules and NTFs are two classes of extracellular ligands that have crucial effects of axonal growth both in vivo and in vitro (Cai et al., 1999;Chen and Strickland, 2003;Ramer et al., 2000). Treatment with NTFs -especially nerve growth factor (NGF) and glial-cell-line-derived neurotrophic factor (GDNF) -is the only known way to induce axonal regeneration into the root entry zone of the spinal cord after dorsal root avulsion (Ramer et al., 2000;Schwab, 2000). GDNF also promotes axonal regeneration in propriospinal neurons after spinal cord injury (Iannotti et al., 2003). Neurturin (NRTN), which is a close homolog of GDNF, restores hindlimb cutan...

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Evidences that β1 integrin and Rac1 are involved in the overriding effect of laminin on myelin-associated glycoprotein inhibitory activity on neuronal cells

Cited by 13 publications

References 55 publications

Neurotrophins support regenerative axon assembly over CSPGs by an ECM-integrin-independent mechanism

Neurotrophins support regenerative axon assembly over CSPGs by an ECM-integrin-independent mechanism

Regulation of axonal outgrowth and pathfinding by integrin–ecm interactions

Neurotrophic factors switch between two signaling pathways that trigger axonal growth

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