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

Mire, Erik; Thomasset, Nicole; Jakeman, Lyn B.; Rougon, Geneviève

doi:10.1016/j.mcn.2007.09.009

Cited by 19 publications

(12 citation statements)

References 50 publications

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“…For the analysis of axon length, the NeuronJ plugin of ImageJ software was used, as previously described [29]. Briefly, the length of a maximum of 40 axons (mean 24.1 ± 1.5 axons) for both normal and underfed was measured for each explants.…”

Section: Methodsmentioning

confidence: 99%

IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

et al. 2017

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Nutrition during the perinatal period programs body growth. Growth hormone (GH) secretion from the pituitary regulates body growth and is controlled by Growth Hormone Releasing Hormone (GHRH) neurons located in the arcuate nucleus of the hypothalamus. We observed that dietary restriction during the early postnatal period (i.e. lactation) in mice influences postnatal growth by permanently altering the development of the somatotropic axis in the pituitary gland. This alteration may be due to a lack of GHRH signaling during this critical developmental period. Indeed, underfed pups showed decreased insulin-like growth factor I (IGF-I) plasma levels, which are associated with lower innervation of the median eminence by GHRH axons at 10 days of age relative to normally fed pups. IGF-I preferentially stimulated axon elongation of GHRH neurons in in vitro arcuate explant cultures from 7 day-old normally fed pups. This IGF-I stimulating effect was selective since other arcuate neurons visualized concomitantly by neurofilament labeling, or AgRP immunochemistry, did not significantly respond to IGF-I stimulation. Moreover, GHRH neurons in explants from age-matched underfed pups lost the capacity to respond to IGF-I stimulation. Molecular analyses indicated that nutritional restriction was associated with impaired activation of AKT. These results highlight a role for IGF-I in axon elongation that appears to be cell selective and participates in the complex cellular mechanisms that link underfeeding during the early postnatal period with programming of the growth trajectory.

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Section: Methodsmentioning

confidence: 99%

IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

et al. 2017

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“…The following groups were assigned: vehicle + spinal cord injury (SCI), TGF-α + SCI, vehicle + laminectomy, TGF-α + laminectomy. Prior studies have shown that the catheter placement in mice results in a local inflammatory response and a transient behavioral impairment, but has no long-term effects on behavioral recovery compared with animals with no catheter (Mire et al, 2008). …”

Section: Methodsmentioning

confidence: 99%

TGF-α increases astrocyte invasion and promotes axonal growth into the lesion following spinal cord injury in mice

White¹,

Yin²,

Jakeman³

2008

Experimental Neurology

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Astrocytes respond to environmental cues and play a multifaceted role in the response to trauma in the central nervous system. As the most prevalent contributors to the glial scar, astrocytes are targeted as barriers to regeneration. However, there is also strong evidence that astrocytes are vital for neuroprotection and metabolic support after injury. In addition, consistent with their role during development, astrocytes may be capable of supporting the growth of injured axons. Therefore, we hypothesized that with appropriate stimulation, the reparative functions of endogenous astrocytes could be harnessed to promote axon growth and recovery after spinal cord injury. Transforming growth factor-α (TGF-α) is a mitogenic growth factor that is active on astrocytes and is poised to contribute to such a strategy. Recombinant TGF-α was administered intrathecally to adult C57BL/6 mice for two weeks following a moderate mid-thoracic spinal cord contusion. By three weeks postinjury, TGF-α infusion had not affected locomotor recovery, but promoted extensive axon growth and altered the composition of the lesion site. The center of the lesion in the treated mice contained greater numbers of new cells and increased astrocyte invasion. Despite the expression of inhibitory proteoglycans, there was a marked increase in axons expressing neurofilament and GAP-43 immunoreactivity, and the new axons were closely associated with increased laminin expression within and beyond the astrocyte matrix. The results demonstrate that astrocytes are dynamic players in the response to spinal cord injury, and the growth supportive role of these cells can be enhanced by TGF-α infusion.

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“…Cultured pyramidal neurons isolated from embryonic hippocampus transfected with the HyPer biosensor were treated in situ with a Sema3A-conditioned medium (300 μg/ml, 20 nM) to promote complete growth cone collapse (N 85%) (Antipenko et al, 2003;Mire et al, 2008). H 2 O 2 production was measured in the same neuron every 30 s during 15 min.…”

Section: Treatment With Wild-type Recombinant Gal-1 Decreases Neuronamentioning

confidence: 99%

Ligand-mediated Galectin-1 endocytosis prevents intraneural H2O2 production promoting F-actin dynamics reactivation and axonal re-growth

Quintá

Wilson

Blidner

et al. 2016

Experimental Neurology

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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

Cited by 19 publications

References 50 publications

IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

IGF-1 Induces GHRH Neuronal Axon Elongation during Early Postnatal Life in Mice

TGF-α increases astrocyte invasion and promotes axonal growth into the lesion following spinal cord injury in mice

Ligand-mediated Galectin-1 endocytosis prevents intraneural H2O2 production promoting F-actin dynamics reactivation and axonal re-growth

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