Regulation of dendritic development by semaphorin 3A through novel intracellular remote signaling

Goshima, Yoshio; Yamashita, Naoya; Nakamura, Fumio; Sasaki, Yukio

doi:10.1080/19336918.2016.1210758

Cited by 37 publications

(35 citation statements)

References 199 publications

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“…Sema3A-induced axonal transport could play an essential role in mediating some of the biological activities of Sema3A (Goshima et al, 2016;Yamashita et al, 2014Yamashita et al, , 2016c. Sema3A signaling at the axonal growth cone is propagated towards the cell body by retrograde axonal transport and drives the AMPA receptor GluA2 to the distal dendrites, thereby regulating dendritic development .…”

Section: Introductionmentioning

confidence: 99%

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Yamane

Yamashita

Hida

et al. 2017

Journal of Cell Science

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Semaphorin3A (Sema3A) is a secreted type of axon guidance molecules that regulates axon wiring through neuropilin-1 (NRP1) and PlexinAs (PlexAs) receptor complex. Sema3A regulates the dendritic branching through a tetrodotoxin (TTX)-sensitive retrograde axonal transport of PlexAs and Tropomyosin-related kinase A (TrkA) complex. We here demonstrate that Nav1.7, a TTX-sensitive Na+ channel, by coupling with collapsin response mediator protein 1 (CRMP1), mediates the Sema3A-induced retrograde transport. In mouse dorsal root ganglion (DRG) neurons, Sema3A increased co-localization of PlexA4 and TrkA in the growth cones and axons. TTX treatment and RNAi knockdown of Nav1.7, sustained Sema3A-induced co-localized signals of PlexA4 and TrkA in growth cones, and suppressed the subsequent localization of PlexA4 and TrkA in distal axons. A similar localization phenotype was observed in crmp1−/− DRG neurons. Sema3A induced co-localization of CRMP1 and Nav1.7 in the growth cones. The half maximal voltage was increased in crmp1−/− neurons when compared to wild-type. In HEK293 cells, introduction of CRMP1 lowered the threshold of the coexpressed Nav1.7. These results suggest that Nav1.7 mediates through coupling with CRMP1 the axonal retrograde signaling of Sema3A.

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Section: Introductionmentioning

confidence: 99%

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Yamane

Yamashita

Hida

et al. 2017

Journal of Cell Science

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“…Synapsis formation of the neuronal network requires local participation of cell adhesion molecules, extracellular proteins, and axon guidance molecules at axodendritic sites [6]. Sema3A and VEGF signaling have been proposed to actively modulate the synaptogenesis and synaptic plasticity, since they are dysregulated in neurological diseases, such as AD [4,16,17].…”

Section: Axonal Degeneration Associated To Synaptogenesis and Synaptimentioning

confidence: 99%

“…Sema3A and VEGF signaling have been proposed to actively modulate the synaptogenesis and synaptic plasticity, since they are dysregulated in neurological diseases, such as AD [4,16,17]. Proper regulation of the synapse formation and dendritic branching contributes to a normal balance between excitatory and inhibitory synaptic transmission; dysregulation of this balance would interfere with the regeneration of damaged CNS axons [6,11,15,27,28].…”

Section: Axonal Degeneration Associated To Synaptogenesis and Synaptimentioning

confidence: 99%

“…In the past decades, an increasing amount of evidence shows that semaphorins participate in refining synaptogenesis, dendritic and axonal exuberance, remodeling of the synaptic network, and even modulating neuronal response to reactive oxygen species and neuronal apoptosis. The association of semaphorins to neuronal function and cell death was soon explored in the context of neurological diseases [2][3][4][5][6]. Several reports linking alteration of semaphorin function or expression in neuropathologies opened an unexplored door to understand the mechanisms and look for treatment alternatives of disorders with unknown or poorly understood pathological origins.…”

Section: Introductionmentioning

confidence: 99%

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Roles of Semaphorins in Neurodegenerative Diseases

Quintremil¹,

Ferrer²,

Puente³

et al. 2019

Neurons - Dendrites and Axons

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Semaphorins are secreted and transmembrane proteins that bind plexin/ neuropilin or integrin receptors, providing paracrine axonal guidance signals and ultimately leading to a functional and developed neuronal network. Following semaphorin's initial discovery, their relevance in the central nervous system (CNS) soon intrigued researchers about the possible links between semaphorins, their receptors and signaling mechanisms and different neurodegenerative diseases. Here, we explore the current knowledge of semaphorin's function and signaling in Alzheimer's disease (AD), Parkinson's disease (PD), Charcot-Marie-Tooth disease (CMT), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP). We focus on the effects of the most known semaphorin subclasses 3A and 4D, yet extending our discussion to other semaphorins that have been found involved in specific neuropathologies and the potential effect of semaphorins modulating the immune system in disorders with inflammatory components. Molecular, cellular, and genetic evidences are reviewed, highlighting the relevance of semaphorins on each disease etiology, pathophysiology, and progression. The newly discovered semaphorin functions in neurological disorders even suggest alternative therapies that may be highly valuable in diseases that have no current cure.

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“…Semaphorin 3A (Sema3A) is an important secreted repulsive guidance factor for many developing neurons [56]. Sema3A may be secreted from non-neuronal cells such as astrocytes.…”

Section: Semaphorin 3amentioning

confidence: 99%

Reactive Astrocyte Gliosis: Production of Inhibitory Molecules

Joghataei¹,

Kazemnejad²,

Mehrabi³

2019

Spinal Cord Injury Therapy [Working Title]

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The astrocytic cell responses to injury have been extensively studied in a variety of experimental models, and the term "astrogliosis" is often used to describe the astrocyte reactions to injury. Cells responding in these ways to injury are often referred to as "reactive astrocytes." Glial scarring appears to be a critical feature of wound healing in the central nervous system (CNS), since elimination of the mitotically active contingent of reactive astrocytes leads to increase in the size of the wound. Reactive astrogliosis is a term coined for the morphological and functional events seen in astrocytes responding to CNS injury. The concept of reactive astrogliosis and its molecular and cellular definition in spinal cord injury (SCI) is still incomplete. Producing several inhibitory molecules discourages regeneration of axons in the injured spinal cord. This inhibition is compounded by the poor regenerative ability of most CNS axons. This is probably a more achievable therapeutic target than axon regeneration, and an effective treatment would be of assistance to the majority of patients with partial cord injuries. Of course, understanding about astrogliosis and producing mediators and inhibitory molecules such as signaling pathways help us to develop new treatment strategies for SCI.

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Regulation of dendritic development by semaphorin 3A through novel intracellular remote signaling

Cited by 37 publications

References 199 publications

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

A functional coupling between CRMP1 and Nav1.7 for retrograde propagation of Semaphorin3A signaling

Roles of Semaphorins in Neurodegenerative Diseases

Reactive Astrocyte Gliosis: Production of Inhibitory Molecules

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