Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

Goldshmit, Yona; Frisca, Frisca; Kaslin, Jan; Pinto, Alexander R.; Tang, Jean Kit; Pébay, Alice; Pinkas‐Kramarski, Ronit; Currie, Peter D.

doi:10.1016/j.neuroscience.2014.12.020

Cited by 12 publications

(6 citation statements)

References 47 publications

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“…Consistent with this beneficial activity of Fgf2, loss of the FGFR signaling antagonist sprouty 2 in mice promotes axon outgrowth and improves the long-distance regeneration of axons (Marvaldi et al, 2015). In response to spinal cord injury, mice lacking sprouty 4 show reduced inflammation and astrocytic gliosis combined with enhanced neuronal survival (Goldshmit et al, 2015). Although sprouty proteins also antagonize signaling by other receptor tyrosine kinases, FGF signaling activation through the loss of sprouty 4 might be particularly important in this situation, as the systemic administration of Fgf2 to wild-type mice with spinal cord injury has the same effect (Goldshmit et al, 2014).…”

Section: Fgfs In Adult Mammalian Nervous System Repairmentioning

confidence: 85%

Fibroblast growth factors: key players in regeneration and tissue repair

2017

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Tissue injury initiates a complex repair process, which in some organisms can lead to the complete regeneration of a tissue. In mammals, however, the repair of most organs is imperfect and results in scar formation. Both regeneration and repair are orchestrated by a highly coordinated interplay of different growth factors and cytokines. Among the key players are the fibroblast growth factors (FGFs), which control the migration, proliferation, differentiation and survival of different cell types. In addition, FGFs influence the expression of other factors involved in the regenerative response. Here, we summarize current knowledge on the roles of endogenous FGFs in regeneration and repair in different organisms and in different tissues and organs. Gaining a better understanding of these FGF activities is important for appropriate modulation of FGF signaling after injury to prevent impaired healing and to promote organ regeneration in humans.

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Section: Fgfs In Adult Mammalian Nervous System Repairmentioning

confidence: 85%

Fibroblast growth factors: key players in regeneration and tissue repair

2017

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“…Studies in both mice and zebrafish have shown that FGF-2 signaling facilitates glial bridge formation following SCI [28,36]. In addition, knockout of spry4, a FGF signaling inhibitor, has been found to reduce inflammatory response and decrease gliosis following SCI [37]. FGF-2 within lipid microtubules has been incorporated into collagen-based hydrogels leading to increased astrocyte infiltration into hydrogels in vitro [38].…”

Section: Role Of Astrocyte Phenotypes In Cns Regenerationmentioning

confidence: 99%

Using biomaterials to promote pro-regenerative glial phenotypes after nervous system injuries

Thompson

Sakiyama‐Elbert

2018

Biomed. Mater.

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Trauma to either the central or peripheral nervous system (PNS) often leads to significant loss of function and disability in patients. This high rate of long-term disability is due to the overall limited regenerative potential of nervous tissue, even though the PNS has more regenerative potential than the central nervous system (CNS). The supporting glial cells in the periphery, Schwann cells, are part of the reason for the improved recovery observed in the PNS. In the CNS, the glial populations, astrocytes and oligodendrocytes (OLs), do not have as much potential to promote regeneration and are at times inhibitory to neuronal growth. In particular, the inhibitory roles astrocytes play following trauma has led to a historical focus on neurons and OLs instead of astrocytes. Recently, this focus has shifted as new, regenerative astrocyte phenotypes have been described. From these observations, glial cells clearly play critical roles in native recovery pathways in both the CNS and PNS. This makes the ability to manipulate both transplanted and native glial cell phenotypes a potentially successful strategy to improve nerve injury outcomes. This review focuses on factors that cause glial cells to adopt repair phenotypes and biomaterials that manipulate and/or harness these glial phenotypes.

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“…Levels of astrocyte-derived chondroitin sulphate proteoglycans (CSPGs) are also markedly decreased, and functional recovery significantly improved [101]. Interestingly, similar effects were observed in the spinal cord of injured mice lacking Spry4, an endogenous feedback inhibitor of FGF signalling [102].…”

Section: Trauma In the Cnsmentioning

confidence: 78%

Fibroblast Growth Factor Signalling in the Diseased Nervous System

Klimaschewski

Claus

2021

Mol Neurobiol

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Fibroblast growth factors (FGFs) act as key signalling molecules in brain development, maintenance, and repair. They influence the intricate relationship between myelinating cells and axons as well as the association of astrocytic and microglial processes with neuronal perikarya and synapses. Advances in molecular genetics and imaging techniques have allowed novel insights into FGF signalling in recent years. Conditional mouse mutants have revealed the functional significance of neuronal and glial FGF receptors, not only in tissue protection, axon regeneration, and glial proliferation but also in instant behavioural changes. This review provides a summary of recent findings regarding the role of FGFs and their receptors in the nervous system and in the pathogenesis of major neurological and psychiatric disorders.

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Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

Cited by 12 publications

References 47 publications

Fibroblast growth factors: key players in regeneration and tissue repair

Fibroblast growth factors: key players in regeneration and tissue repair

Using biomaterials to promote pro-regenerative glial phenotypes after nervous system injuries

Fibroblast Growth Factor Signalling in the Diseased Nervous System

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