α4 Integrin Is Expressed during Peripheral Nerve Regeneration and Enhances Neurite Outgrowth

Vogelezang, Mariette G.; Liu, Zhiqiang; Relvas, João B.; Raivich, Gennadij; Scherer, Steven S.; ffrench‐Constant, Charles

doi:10.1523/jneurosci.21-17-06732.2001

Cited by 75 publications

(72 citation statements)

References 55 publications

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“…␣4 and ␣5 integrin constructs were produced as previously described (Vogelezang et al, 2001). Generation of human ␣9 integrin missing the cytoplasmic domain was constructed by introducing a HindIII restriction site 10 bp proximal to the ATG start codon of ␣9 and a stop codon 2 amino acids after the transmembrane domain followed by a NotI restriction site before the GFFKR motif deleted the ␣9 protein.…”

Section: Integrin Constructs and Chimerasmentioning

confidence: 99%

“…They promote neurite outgrowth in embryonic (Lein et al, 1991;Neugebauer et al, 1991), postnatal (Tomaselli et al, 1993;Vogelezang et al, 2001), and adult neurons (Condic 2001;Gardiner et al, 2005), and are involved in peripheral nerve regeneration (Vogelezang et al, 2001;Gardiner et al, 2005Gardiner et al, , 2007. After development, some integrin receptors are downregulated, resulting in adult neurons that are unable to interact with certain matrix molecules, including TN-C (Jones, 1996;Pinkstaff et al, 1999), and cells may lose the ability to regulate surface integrin levels to optimize cell-matrix interactions.…”

Section: Introductionmentioning

confidence: 99%

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

Andrews¹,

Czvitkovich²,

Dassie³

et al. 2009

J. Neurosci.

149

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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Section: Integrin Constructs and Chimerasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Andrews¹,

Czvitkovich²,

Dassie³

et al. 2009

J. Neurosci.

149

162

View full text Add to dashboard Cite

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“…Sections (40 m) were cut through the facial nucleus and all sections (the facial nucleus is Ϸ700 m in length in the anterior-posterior direction) were mounted and stained with neutral red. All neuronal profiles in every section were counted and total counts corrected by using the Abercrombie correction (40).…”

Section: Detection Of ␤-Galactosidasementioning

confidence: 99%

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Tebar

Géranton

Parsons-Perez

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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A large number of cytokines and growth factors support the development and subsequent maintenance of postnatal motor neurons. RegIII␤, also known as Reg2 in rat and HIP/PAP1 in humans, is a member of a family of growth factors found in many areas of the body and previously shown to play an important role in both the development and regeneration of subsets of motor neurons. It has been suggested that RegIII␤ expressed by motor neurons is both an obligatory intermediate in the downstream signaling of the leukemia inhibitory factor/ciliary neurotrophic factor (CNTF) family of cytokines, maintaining the integrity of motor neurons during development, as well as a powerful influence on Schwann cell growth during regeneration of the peripheral nerve. Here we report that in mice with a deletion of the RegIII␤ gene, motor neuron survival was unaffected up to 28 weeks after birth. However, there was no CNTF-mediated rescue of neonatal facial motor neurons after axotomy in KO animals when compared with wild-type. In mice, RegIII␤ positive motor neurons are concentrated in cranial motor nuclei that are involved in the patterning of swallowing and suckling. We found that suckling was impaired in RegIII␤ KO mice and correlated this with a significant delay in myelination of the hypoglossal nerve. In summary, we propose that RegIII␤ has an important role to play in the developmental fine-tuning of neonatal motor behaviors mediating the response to peripherally derived cytokines and growth factors and regulating the myelination of motor axons.Schwann cells ͉ suckling ͉ hypoglossal nerve ͉ LIF

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“…The integrin ␣4␤1 has been studied extensively with respect to its role in inflammation and hematopoiesis (Lobb and Hemler, 1994;Arroyo et al, 1996), and more recently, it has been shown to function in neurons (Vogelezang et al, 2001;Wingerd et al, 2002). The ␣4␤1 integrin binds multiple ligands, including vascular cell adhesion molecule-1 (VCAM-1; Osborn et al, 1989), fibronectin's connecting sequence-1 (CS-1; Guan and Hynes, 1990), thrombospondin-1 (Yabkowitz et al, 1993), other ␣4 integrins (Altevogt et al, 1995), the propolypeptide of von Willebrand factor (Isobe et al, 1997), ICAM-4 (Spring et al, 2001), transglutaminase C (Isobe et al, 1999), and osteopontin (Bayless et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…The ␣4␤1 integrin binds multiple ligands, including vascular cell adhesion molecule-1 (VCAM-1; Osborn et al, 1989), fibronectin's connecting sequence-1 (CS-1; Guan and Hynes, 1990), thrombospondin-1 (Yabkowitz et al, 1993), other ␣4 integrins (Altevogt et al, 1995), the propolypeptide of von Willebrand factor (Isobe et al, 1997), ICAM-4 (Spring et al, 2001), transglutaminase C (Isobe et al, 1999), and osteopontin (Bayless et al, 1998). Neural cells that express ␣4␤1 include neural crest cells (Kil et al, 1998), retinal cells (Sheppard et al, 1994;Cann et al, 1996;Hikita et al, 2003), dorsal root ganglion neurons (Vogelezang et al, 2001), and SCG neurons (Vogelezang et al, 2001;Wingerd et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Expression and function of integrin α4β1 and vascular cell adhesion molecule‐1 (VCAM‐1) during sympathetic innervation of the heart

Wingerd

Goodman

Leu

et al. 2004

Developmental Dynamics

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The interaction between the integrin ␣4␤1 receptor on superior cervical ganglion (SCG) neurons and vascular cell adhesion molecule-1 (VCAM-1) in cardiac tissue has been implicated in proper development of the sympathetic innervation of the heart (Wingerd et al.[2002] J Neurosci 22:10772-10780). In this study, we examined the expression and function of ␣4␤1 and VCAM-1 in developing rat SCG and heart. In vitro, the ␣4␤1-dependent neurite outgrowth on VCAM-1 decreased by approximately 50% from postnatal day 1 to 6. This down-regulation was correlated with a shift in ␣4 isoform and a shift in ␣4 localization from neurites to cell bodies. This altered localization was also observed in vivo but on a different time scale. ␣4 was detected on most developing SCG neurons and on macrophages and blood vessels. In the heart, ␣4 was detected on sympathetic axons, but the percentage of ␣4-positive fibers decreased with age. VCAM-1 immunoreactivity was abundant in heart tissue throughout development, in close proximity to sympathetic axons. The regulation of ␣4␤1 function, and localization of ␣4 and VCAM-1, are consistent with a role for the ␣4␤1-VCAM-1 interaction in extension of sympathetic axons into the myocardium. Developmental Dynamics 231:359 -369, 2004.

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α4 Integrin Is Expressed during Peripheral Nerve Regeneration and Enhances Neurite Outgrowth

Cited by 75 publications

References 55 publications

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

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

Deletion of the mouse RegIIIβ (Reg2) gene disrupts ciliary neurotrophic factor signaling and delays myelination of mouse cranial motor neurons

Expression and function of integrin α4β1 and vascular cell adhesion molecule‐1 (VCAM‐1) during sympathetic innervation of the heart

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