Neurite outgrowth on a fibronectin isoform expressed during peripheral nerve regeneration is mediated by the interaction of paxillin with α4β1 integrins

Vogelezang, Mariette G.; Förster, Ulrike; Han, Jaewon; Ginsberg, Mark H.; ffrench‐Constant, Charles

doi:10.1186/1471-2202-8-44

Cited by 23 publications

(16 citation statements)

References 51 publications

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“…To date, four laminin-binding b1-associated integrins: a1b1, a3b1, a6b1, and a7b1 integrins have been identified in adult DRG (Lefcort et al, 1992;Vogelezang et al, 2001;Wallquist et al, 2004). Culture studies using function-blocking antibodies have revealed the b1-associated integrins to be functionally important in mediating adhesion and neurite outgrowth on laminin in vitro (Tomaselli et al, 1993;Condic and Letourneau, 1997;Agius and Cochard, 1998;Ivins et al, 2000;Ekstrom et al, 2003;Gardiner et al, 2005;Vogelezang et al, 2007), with a7b1 and a3b1 integrin mediating neurite outgrowth from adult mouse sensory neurons on laminins-111 and -211 and a6b1 integrin mediating outgrowth on laminins-411 and -511 (Plantman et al, 2008).…”

Section: With Permission Copyright Elsevier (2007)mentioning

confidence: 95%

“…Fibronectin is expressed at relatively low levels in the Schwann cell basement membrane of adult peripheral nerves Lefcort et al, 1992), but is rapidly upregulated following injury in the PNS (Lefcort et al, 1992) and CNS (Tom et al, 2004), either deposited from plasma or synthesized by fibroblasts and endothelial cells. Fibronectin acts as a substratum for migrating Schwann cells is a chemoattractant, and mitogen (Baron- Van Evercooren et al, 1982b), and also provides a direct substrate for adhesion and outgrowth of regenerating axons (Baron-Van Evercooren et al, 1982a;Rogers et al, 1983;Vogelezang et al, 2001Vogelezang et al, , 2007Gardiner et al, 2007). Following nerve injury, embryonic isoforms of fibronectin which include the V (\variable in length") region (also known as the type III connecting segment \IIICS" [Fig.…”

Section: Integrin-ecm Interactions During Regeneration Of the Somatosmentioning

confidence: 99%

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Integrins and the extracellular matrix: Key mediators of development and regeneration of the sensory nervous system

Gardiner

2011

Developmental Neurobiology

115

101

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The somatosensory nervous system is responsible for the transmission of a multitude of sensory information from specialized receptors in the periphery to the central nervous system. Sensory afferents can potentially be damaged at several sites: in the peripheral nerve; the dorsal root; or the dorsal columns of the spinal cord; and the success of regeneration depends on the site of injury. The regeneration of peripheral nerve branches following injury is relatively successful compared to central branches. This is largely attributed to the presence of neurotrophic factors and a Schwann cell basement membrane rich in permissive extracellular matrix (ECM) components which promote axonal regeneration in the peripheral nerve. Modulation of the ECM environment and/or neuronal integrins may enhance regenerative potential of sensory neurons following peripheral or central nerve injury or disease. This review describes the interactions between integrins and ECM molecules (particularly the growth supportive ligands, laminin, and fibronectin; and the growth inhibitory chondroitin sulfate proteoglycans (CSPGs)) during development and regeneration of sensory neurons following physical injury or neuropathy.

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Section: With Permission Copyright Elsevier (2007)mentioning

confidence: 95%

Section: Integrin-ecm Interactions During Regeneration Of the Somatosmentioning

confidence: 99%

Integrins and the extracellular matrix: Key mediators of development and regeneration of the sensory nervous system

Gardiner

2011

Developmental Neurobiology

115

101

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“…Previous studies by Vogelezang et al (2001Vogelezang et al ( , 2007 determined the ␣4 integrin cytoplasmic domain to be necessary for neurite outgrowth from PC12 cells on fibronectin. To determine the contribution of extracellular and cytoplasmic domains of ␣9 integrin to neurite outgrowth on TN-C, chimeric constructs of different integrin domains were tested.…”

Section: Expression Of ␣9 Integrin In Pc12 Cells Overcomes Inhibitionmentioning

confidence: 99%

α9 Integrin Promotes Neurite Outgrowth on Tenascin-C and Enhances Sensory Axon Regeneration

Andrews¹,

Czvitkovich²,

Dassie³

et al. 2009

J. Neurosci.

146

162

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Damaged CNS axons are prevented from regenerating by an environment containing many inhibitory factors. They also lack an integrin that interacts with tenascin-C, the main extracellular matrix glycoprotein of the CNS, which is upregulated after injury. The ␣9␤1 integrin heterodimer is a receptor for the nonalternatively spliced region of tenascin-C, but the ␣9 subunit is absent in adult neurons. In this study, we show that PC12 cells and adult rat dorsal root ganglion (DRG) neurons do not extend neurites on tenascin-C. However, after forced expression of ␣9 integrin, extensive neurite outgrowth from PC12 cells and adult rat DRG neurons occurs. Moreover, both DRG neurons and PC12 cells secrete tenascin-C, enabling ␣9-transfected cells to grow axons on tissue culture plastic. Using adeno-associated viruses to express ␣9 integrin in vivo in DRGs, we examined axonal regeneration after cervical dorsal rhizotomy or dorsal column crush in the adult rat. After rhizotomy, significantly more dorsal root axons regrew into the dorsal root entry zone at 6 weeks after injury in ␣9 integrinexpressing animals than in green fluorescent protein (GFP) controls. Similarly, after a dorsal column crush injury, there was significantly more axonal growth into the lesion site compared with GFP controls at 6 weeks after injury. Behavioral analysis after spinal cord injury revealed that both experimental and control groups had an increased withdrawal latency in response to mechanical stimulation when compared with sham controls; however, in response to heat stimulation, normal withdrawal latencies returned after ␣9 integrin treatment but remained elevated in control groups.

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“…Proteins for neurotransmission reach the presynaptic axon terminal, whereas those intended for postsynaptic functions are restricted to dendrites (Conde and Caceres, 2009;Hirokawa et al, 2009;Lasiecka and Winckler, 2011;Farías et al, 2012). Integrins are growth and survival molecules that are important for axon growth during development and for regeneration in the peripheral nervous system (PNS) in adulthood (Werner et al, 2000;Vogelezang et al, 2001Vogelezang et al, , 2007Gardiner et al, 2005). During CNS development, they are involved in axon growth and guidance (Huang et al, 2006;Myers et al, 2011) and, in adulthood, they regulate aspects of synaptic plasticity (McGeachie et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Exclusion of Integrins from CNS Axons Is Regulated by Arf6 Activation and the AIS

et al. 2015

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Integrins are adhesion and survival molecules involved in axon growth during CNS development, as well as axon regeneration after injury in the peripheral nervous system (PNS). Adult CNS axons do not regenerate after injury, partly due to a low intrinsic growth capacity. We have previously studied the role of integrins in axon growth in PNS axons; in the present study, we investigate whether integrin mechanisms involved in PNS regeneration may be altered or lacking from mature CNS axons by studying maturing CNS neurons in vitro. In rat cortical neurons, we find that integrins are present in axons during initial growth but later become restricted to the somato-dendritic domain. We investigated how this occurs and whether it can be altered to enhance axonal growth potential. We find a developmental change in integrin trafficking; transport becomes predominantly retrograde throughout axons, but not dendrites, as neurons mature. The directionality of transport is controlled through the activation state of ARF6, with developmental upregulation of the ARF6 GEF ARNO enhancing retrograde transport. Lowering ARF6 activity in mature neurons restores anterograde integrin flow, allows transport into axons, and increases axon growth. In addition, we found that the axon initial segment is partly responsible for exclusion of integrins and removal of this structure allows integrins into axons. Changing posttranslational modifications of tubulin with taxol also allows integrins into the proximal axon. The experiments suggest that the developmental loss of regenerative ability in CNS axons is due to exclusion of growth-related molecules due to changes in trafficking.

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Neurite outgrowth on a fibronectin isoform expressed during peripheral nerve regeneration is mediated by the interaction of paxillin with α4β1 integrins

Cited by 23 publications

References 51 publications

Integrins and the extracellular matrix: Key mediators of development and regeneration of the sensory nervous system

Integrins and the extracellular matrix: Key mediators of development and regeneration of the sensory nervous system

α9 Integrin Promotes Neurite Outgrowth on Tenascin-C and Enhances Sensory Axon Regeneration

Exclusion of Integrins from CNS Axons Is Regulated by Arf6 Activation and the AIS

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