Functional Interaction between Matrix Metalloproteinase-3 and Semaphorin-3C during Cortical Axonal Growth and Guidance

Gonthier, B.; Nasarre, Cécile; Roth, Lise; Perraut, Martine; Thomasset, Nicole; Roussel, G.; Aunis, Dominique; Bagnard, Dominique

doi:10.1093/cercor/bhl082

Cited by 42 publications

(34 citation statements)

References 47 publications

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“…For instance, LGI1 expression down-regulates ROBO1 (Kunapuli et al, 2010), the receptor for the SLIT protein which functions as a repulsive cue for neurite branching and outgrowth. LGI1 also reduces matrix metalloproteinases (Kunapuli et al, 2004), which have been implicated in axon outgrowth (Gonthier et al, 2007). In addition, LGI1 was recently shown to have a high binding affinity for a Nogo receptor (NogoR1) (Thomas et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Epilepsy GeneLGI1Regulates Postnatal Developmental Remodeling of Retinogeniculate Synapses

Zhou¹,

Zhang²,

Ozkaynak³

et al. 2012

J. Neurosci.

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Retinogeniculate connections undergo postnatal refinement in the developing visual system. Here we report that non-ion channel epilepsy gene LGI1, mutated in human autosomal dominant lateral temporal lobe epilepsy (ADLTE), regulates postnatal pruning of retinal axons in visual relay thalamus. By introducing an ADLTE-associated truncated mutant LGI1 (836delC) or excess full-length LGI1 into transgenic mice, we found that mutant LGI1 blocks, while excess LGI1 accelerates retinogeniculate axon pruning. The normal postnatal single fiber strengthening was arrested by mutant LGI1, and contrastingly, was enhanced by excess wild-type LGI1. The maximum response of the retinogeniculate synapses, on the other hand, remained the same in mature LGI1 transgenic mice, indicating that mutant LGI1 blocks, whereas excess wild-type LGI1 promotes, weak axon fiber elimination. Heterozygous deletion of the LGI1 gene, as found in ADLTE patients, inhibited postnatal retinogeniculate synapse elimination, an effect similar to the ADLTE truncated mutant LGI1. The results identify sensory axon remodeling defects in a sensory aura-associated human epilepsy disorder.

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Section: Discussionmentioning

confidence: 99%

Epilepsy GeneLGI1Regulates Postnatal Developmental Remodeling of Retinogeniculate Synapses

Zhou¹,

Zhang²,

Ozkaynak³

et al. 2012

J. Neurosci.

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“…Strikingly, the expression of Sema3A in the marginal zone is also implicated in cortical dendrite development, orienting them to the pial surface [32] and promoting their outgrowth and branching [33]. Interestingly, the growth promoting effect of semaphorins in the cortex relates to specific activation of matrix metalloproteinases [34]. Thus, the spatial and temporal regulation of semaphorin expression is the source of precise wiring.…”

Section: Sema3amentioning

confidence: 99%

The many faces of semaphorins: from development to pathology

Roth

Koncina

Šatkauskas

et al. 2008

Cell. Mol. Life Sci.

159

144

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The semaphorin family is a large group of proteins controlling cell migration and axonal growth cone guidance. These proteins are bi-functional signals capable of growth promotion or growth inhibition. Initially described in the nervous system, the majority of studies related to semaphorins and semaphorin signalling are nowadays performed in model systems outside the nervous system. Here, we provide an exhaustive review of the many faces of semaphorins both during developmental, regulatory and pathological processes. Indeed, because of their crucial fundamental roles, the semaphorins and their receptors represent important targets for the development of drugs directed at a variety of diseases.

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“…They interact with a wide range of substrates (e.g., extracellular matrix proteins, cytokines, growth factors, cell adhesion molecules, receptors), which confer to MMPs broad functional diversity (Rivera et al, 2010). They are thus involved in numerous pathological and physiological processes: neural cell motility and outgrowth (Ogier et al, 2006; Gonthier et al, 2007; Ould-yahoui et al, 2009), neuronal death (Jourquin et al, 2003), synaptic plasticity and cognition (Jourquin et al, 2005; Chaillan et al, 2006; Meighan et al, 2006; Nagy et al, 2006; Kaliszewska et al, 2012), neuroinflammation (Ogier et al, 2005; Hu et al, 2007; Candelario-Jalil et al, 2009) and blood brain barrier (BBB) breakdown (Yang et al, 2007). …”

Section: Introductionmentioning

confidence: 99%

Differential spatio-temporal regulation of MMPs in the 5xFAD mouse model of Alzheimerâ€™s disease: evidence for a pro-amyloidogenic role of MT1-MMP

Bonnet

Bernard

et al. 2014

Front. Aging Neurosci.

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Matrix metalloproteinases (MMPs) are pleiotropic endopeptidases involved in a variety of neurodegenerative/neuroinflammatory processes through their interactions with a large number of substrates. Among those, the amyloid precursor protein (APP) and the beta amyloid peptide (Aβ) are largely associated with the development of Alzheimer’s disease (AD). However, the regulation and potential contribution of MMPs to AD remains unclear. In this study, we investigated the evolution of the expression of MMP-2, MMP-9, and membrane-type 1-MMP (MT1-MMP) in the hippocampus at different stages of the pathology (asymptomatic, prodromal-like and symptomatic) in the 5xFAD transgenic mouse AD model. In parallel we also followed the expression of functionally associated factors. Overall, the expression of MMP-2, MMP-9, and MT1-MMP was upregulated concomitantly with the tissue inhibitor of MMPs-1 (TIMP-1) and several markers of inflammatory/glial response. The three MMPs exhibited age- and cell-dependent upregulation of their expression, with MMP-2 and MMP-9 being primarily located to astrocytes, and MT1-MMP to neurons. MMP-9 and MT1-MMP were also prominently present in amyloid plaques. The levels of active MT1-MMP were highly upregulated in membrane-enriched fractions of hippocampus at 6 months of age (symptomatic phase), when the levels of APP, its metabolites APP C-terminal fragments (CTFs), and Aβ trimers were the highest. Overexpression of MT1-MMP in HEK cells carrying the human APP Swedish mutation (HEKswe) strongly increased β-secretase derived C-terminal APP fragment (C99) and Aβ levels, whereas MMP-2 overexpression nearly abolished Aβ production without affecting C99. Our data consolidate the emerging idea of a regulatory interplay between MMPs and the APP/Aβ system, and demonstrate for the first time the pro-amyloidogenic features of MT1-MMP. Further investigation will be justified to evaluate this MMP as a novel potential therapeutic target in AD.

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Functional Interaction between Matrix Metalloproteinase-3 and Semaphorin-3C during Cortical Axonal Growth and Guidance

Cited by 42 publications

References 47 publications

Epilepsy GeneLGI1Regulates Postnatal Developmental Remodeling of Retinogeniculate Synapses

Epilepsy GeneLGI1Regulates Postnatal Developmental Remodeling of Retinogeniculate Synapses

The many faces of semaphorins: from development to pathology

Differential spatio-temporal regulation of MMPs in the 5xFAD mouse model of Alzheimerâ€™s disease: evidence for a pro-amyloidogenic role of MT1-MMP

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