Regulation of neuropilin 1 by spinal cord injury in adult rats

Agudo, Marta; Robinson, Michelle; Cafferty, William B. J.; Bradbury, Elizabeth J.; Kilkenny, Carol; Hunt, Stephen P.; McMahon, Stephen B.

doi:10.1016/j.mcn.2004.10.008

Cited by 15 publications

(11 citation statements)

References 41 publications

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“…However, this conversion needs the presence of three partners precisely localized: L1 and Nrp1 on the axonal growth cone, and Sema3A in the environment. Our results and previous data in literature describes these partners in the appropriate locations: Sema3A in the scar and L1 and Nrp1 in cortical and sensory neurons (De Winter et al, 2002;Akopians et al, 2003;de Wit and Verhaagen, 2003;Hashimoto et al, 2004;Agudo et al, 2005).…”

Section: Discussionsupporting

confidence: 83%

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Modulating Sema3A signal with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury

Mire

Thomasset

Jakeman

et al. 2008

Molecular and Cellular Neuroscience

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We examined whether Sema3A which is upregulated at the site of spinal cord injury exerts a direct effect on axons. We used ASNKL peptide that prevents specifically the inhibitory effect of Sema3A on L1/Neuropilin1 (Nrp1) expressing axons. In the naïve mouse spinal cord, L1 is located on a subset of corticospinal axons, whereas Nrp1 is barely detectable. After contusion injury, Nrp1 is found on L1-negative immune cells whereas its expression does not increase on severed axons. L1 expressing axons sprout extensively into the lesion site but no difference in axon density could be detected in the lesion area of mice treated with ASNKL. In agreement, these mice did not recover a better motor function than controls. Similarly, culture of neurons sensitive to ASNKL on cryosections of lesioned spinal cords revealed no effect of Sema3A. Our data indicate a limited direct effect of Sema3A on axonal growth at the site of a contusion injury, and suggest that alternative mechanisms underlie positive effects of Sema3A inhibition on motor recovery.

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Section: Discussionsupporting

confidence: 83%

“…3E and H). As for rats (Agudo et al, 2005), blood vessels were also detected with both antibodies ( fig. 3F and I).…”

Section: Expression Of L1 and Nrp1 In The Naïve Spinal Cordmentioning

confidence: 75%

Modulating Sema3A signal with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury

Mire

Thomasset

Jakeman

et al. 2008

Molecular and Cellular Neuroscience

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“…For example, it has been shown that the effect of VEGF-A on the growth of sensory axons is mediated through the activation of VEGFR2 (Sondell et al, 2000). When binding to axonal neuropilins (Agudo et al, 2005), VEGF competes with semaphorins, which are known to have negative effects on axonal guidance and growth (Hou et al, 2008). It has already been shown that overexpression of semaphorin 3A in injured spinal cords significantly inhibits excessive sprouting of sensory unmyelinated fibers and reduces mechanical allodynia (Cameron et al, 2006;Rabchevsky, 2006;Tang et al, 2004).…”

Section: Axonal Sprouting and Sci Painmentioning

confidence: 99%

Vascular Endothelial Growth Factor and Spinal Cord Injury Pain

Nešić

Sundberg

Herrera

et al. 2010

Journal of Neurotrauma

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Vascular endothelial growth factor (VEGF)-A mRNA was previously identified as one of the significantly upregulated transcripts in spinal cord injured tissue from adult rats that developed allodynia. To characterize the role of VEGF-A in the development of pain in spinal cord injury (SCI), we analyzed mechanical allodynia in SCI rats that were treated with either vehicle, VEGF-A isoform 165 (VEGF 165 ), or neutralizing VEGF 165 -specific antibody. We have observed that exogenous administration of VEGF 165 increased both the number of SCI rats that develop persistent mechanical allodynia, and the level of hypersensitivity to mechanical stimuli. Our analysis identified excessive and aberrant growth of myelinated axons in dorsal horns and dorsal columns of chronically injured spinal cords as possible mechanisms for both SCI pain and VEGF 165 -induced amplification of SCI pain, suggesting that elevated endogenous VEGF 165 may have a role in the development of allodynia after SCI. However, the neutralizing VEGF 165 antibody showed no effect on allodynia or axonal sprouting after SCI. It is possible that another endogenous VEGF isoform activates the same signaling pathway as the exogenouslyadministered 165 isoform and contributes to SCI pain. Our transcriptional analysis revealed that endogenous VEGF 188 is likely to be the isoform involved in the development of allodynia after SCI. To the best of our knowledge, this is the first study to suggest a possible link between VEGF, nonspecific sprouting of myelinated axons, and mechanical allodynia following SCI.

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“…Second, meningeal fibroblast-derived Sema3A inhibits DRG axon growth in vitro, and antibodies capable of blocking neuropilin function promote axon growth in an in vitro model of the CNS scar Shearer et al, 2003). Third, adult CNS and PNS neurons express neuropilins, plexinAs, CRMPs, and MICALs, and sprouting sensory axons are responsive to Sema3-mediated axon repulsion in vitro and in vivo (Agudo et al, 2005;De Winter et al, 2002b;Gavazzi et al, 2000;Lindholm et al, 2004;Owesson et al, 2000;Pasterkamp et al, 1998aPasterkamp et al, ,b, 2000Reza et al, 1999;Tanelian et al, 1997;Tang et al, 2004;Wang and Strittmatter, 1996). Fourth, conditioning peripheral nerve injuries that allow DRG axons to regenerate centrally do not promote regenerative axon growth through Sema3-expressing scar tissue (Pasterkamp et al, 2001).…”

Section: Egcg Neutralizes Axon Repulsion By Sema3smentioning

confidence: 99%