Fibroblast Growth Factor and Insulin-Like Growth Factor Rescue Growth Cones of Sensory Neurites from Collapse After Tetracaine-Induced Injury

Seki, Tomoko; Nazeer, A. Abdel; Sekimoto, Kenichi; Guao, Yao; Al-Jahdari, Wael S.; Saito, Shigeru

doi:10.1213/ane.0b013e3181d31ea6

Cited by 11 publications

(5 citation statements)

References 29 publications

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“…FGF-2 also interacts with other GFs in lesion regions to promote multiple biological effects. Seki et al found that the application of FGF-2 and IGF in different ratios resulted in different degrees of rescued growth cone collapse in sensory neurons [ 135 ]. In addition, the administration of exogenous FGF-2 benefited interleukin-6 and its related receptor expression in differentiated and proliferating SCs, respectively [ 136 ].…”

Section: The Roles Of Ngf and Fgf-2 In Pnimentioning

confidence: 99%

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

et al. 2020

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Peripheral nerve injury (PNI), one of the most common concerns following trauma, can result in a significant loss of sensory or motor function. Restoration of the injured nerves requires a complex cellular and molecular response to rebuild the functional axons so that they can accurately connect with their original targets. However, there is no optimized therapy for complete recovery after PNI. Supplementation with exogenous growth factors (GFs) is an emerging and versatile therapeutic strategy for promoting nerve regeneration and functional recovery. GFs activate the downstream targets of various signaling cascades through binding with their corresponding receptors to exert their multiple effects on neurorestoration and tissue regeneration. However, the simple administration of GFs is insufficient for reconstructing PNI due to their short half-life and rapid deactivation in body fluids. To overcome these shortcomings, several nerve conduits derived from biological tissue or synthetic materials have been developed. Their good biocompatibility and biofunctionality made them a suitable vehicle for the delivery of multiple GFs to support peripheral nerve regeneration. After repairing nerve defects, the controlled release of GFs from the conduit structures is able to continuously improve axonal regeneration and functional outcome. Thus, therapies with growth factor (GF) delivery systems have received increasing attention in recent years. Here, we mainly review the therapeutic capacity of GFs and their incorporation into nerve guides for repairing PNI. In addition, the possible receptors and signaling mechanisms of the GF family exerting their biological effects are also emphasized.

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Section: The Roles Of Ngf and Fgf-2 In Pnimentioning

confidence: 99%

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

et al. 2020

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“…During the axonal regeneration, IGF-1 has been shown to play a critical role in SCs by promoting their survival, proliferation, maturation, and differentiation to myelinating phenotypes 33 – 35 . IGF-1 has been also reported to increase the survival and axonal outgrowth of neurons 36 – 38 . Our work firstly investigated the target regulation of miR-129 in affecting regenerative microenvironment to further regulate the proliferation and migration of primary SCs, and neurite outgrowth of DRG neurons.…”

Section: Discussionmentioning

confidence: 98%

miR-129 controls axonal regeneration via regulating insulin-like growth factor-1 in peripheral nerve injury

et al. 2018

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The microenvironment of peripheral nerve regeneration consists of multiple neurotrophic factors, adhesion molecules, and extracellular matrix molecules, secreted by unique glial cells in the peripheral nerve system (PNS)-Schwann cell (SCs). Following peripheral nerve injury (PNI), local IGF-1 production is upregulated in SCs and denervated muscle during axonal sprouting and regeneration. Regulation of IGF-1/IGF-1R signaling is considered as a potentially targeted therapy of PNI. We previously identified a group of novel miRNAs in proximal nerve following rat sciatic nerve transection. The present work focused on the role of miR-129 in regulation of IGF-1 signaling after sciatic nerve injury. The temporal change profile of the miR-129 expression was negatively correlated with the IGF-1 expression in proximal nerve stump and dorsal root ganglion (DRG) following sciatic nerve transection. An increased expression of miR-129 inhibited proliferation and migration of SCs, and axonal outgrowth of DRG neurons, which was inversely promoted by silencing of the miR-129 expression. The IGF-1 was identified as one of the multiple target genes of miR-129, which exerted negative regulation of IGF-1 by translational suppression. Moreover, knockdown of IGF-1 attenuated the promoting effects of miR-129 inhibitor on proliferation and migration of SCs, and neurite outgrowth of DRG neurons. Overall, our data indicated that miR-129 own the potential to regulate the proliferation and migration of SCs by targeting IGF-1, providing further insight into the regulatory role of miRNAs in peripheral nerve regeneration. The present work not only provides new insight into miR-129 regulation of peripheral nerve regeneration by robust phenotypic modulation of neural cells, but also opens a novel therapeutic window for PNI by mediating IGF-1 production. Our results may provide further experimental basis for translation of the molecular therapy into the clinic.

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“…IGF-1 is a basic peptide composed of 70 amino acids with a variety of functions in neuronal cells ( Zheng and Quirion, 2006 ; Croci et al ., 2011 ). IGF-1 plays an important role in promoting axonal growth from DRG neurons ( Bomze et al ., 2001 ; Jones et al ., 2003 ; Seki et al ., 2010 ) and supports to a population of predominantly nociceptive neurons in DRG which may contribute to neuropathic pain ( Craner et al ., 2002 ; Miura et al ., 2011 ). Exogenous administration of IGF-1 after injury is neuroprotective and improves long-term neurological function ( Guan, 2008 ).…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of IGF-1 on Different Subpopulations of DRG Neurons with Neurotoxicity Induced by gp120 and Dideoxycytidine In Vitro

Lin

Dong

Liu

et al. 2014

Biomolecules & Therapeutics

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Peripheral neuropathy induced by human immunodeficiency virus (HIV) infection and antiretroviral therapy is not only difficult to distinguish in clinical practice, but also difficult to relieve the pain symptoms by analgesics because of the severity of the disease at the later stage. Hence, to explore the mechanisms of HIV-related neuropathy and find new therapeutic options are particularly important for relieving neuropathic pain symptoms of the patients. In the present study, primary cultured embryonic rat dorsal root ganglion (DRG) neurons were used to determine the neurotoxic effects of HIV-gp120 protein and/or antiretroviral drug dideoxycytidine (ddC) and the therapeutic actions of insulin-like growth factor-1 (IGF-1) on gp120- or ddC-induced neurotoxicity. DRG neurons were exposed to gp120 (500 pmol/L), ddC (50 μmol/L), gp120 (500 pmol/L) plus ddC (50 μmol/L), gp120 (500 pmol/L) plus IGF-1 (20 nmol/L), ddC (50 μmol/L) plus IGF-1 (20 nmol/L), gp120 (500 pmol/L) plus ddC (50 μmol/L) plus IGF-1 (20 nmol/L), respectively, for 72 hours. The results showed that gp120 and/or ddC caused neurotoxicity of primary cultured DRG neurons. Interestingly, the severity of neurotoxicity induced by gp120 and ddC was different in different subpopulation of DRG neurons. gp120 mainly affected large diameter DRG neurons (>25 μm), whereas ddC mainly affected small diameter DRG neurons (≤25 μm). IGF-1 could reverse the neurotoxicity induced by gp120 and/or ddC on small, but not large, DRG neurons. These data provide new insights in elucidating the pathogenesis of HIV infection- or antiretroviral therapy-related peripheral neuropathy and facilitating the development of novel treatment strategies.

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Fibroblast Growth Factor and Insulin-Like Growth Factor Rescue Growth Cones of Sensory Neurites from Collapse After Tetracaine-Induced Injury

Abstract: bFGF and bIGF decreased growth cone collapse after tetracaine-induced injury in vitro.

Cited by 11 publications

References 29 publications

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

miR-129 controls axonal regeneration via regulating insulin-like growth factor-1 in peripheral nerve injury

The Protective Effects of IGF-1 on Different Subpopulations of DRG Neurons with Neurotoxicity Induced by gp120 and Dideoxycytidine In Vitro

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