The glial scar in spinal cord injury and repair

Yuan, Yihang; He, Cheng

doi:10.1007/s12264-013-1358-3

Cited by 166 publications

(119 citation statements)

References 134 publications

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“…At the same time, the glial scar provides a barrier against inflammation to limit secondary injury, and this is beneficial [10,11] . Cheng He of the Second Military Medical University (Shanghai) [12] discusses the complex role of the glial scar in influencing axon regeneration and neuroinflammation. The choice of appropriate experimental systems and species for SCI research is crucial.…”

Section: Sci Is a Complex Condition It Involves Damage Tomentioning

confidence: 99%

An update on spinal cord injury research

Zou

2013

Neurosci. Bull.

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Spinal cord injury (SCI) is an ever-increasing challenge.Severe injury can cause long-term loss of sensory and motor functions, as well as other chronic conditions, such as neuropathic pain and autonomic dysreflexia. So far, most research has been focused on acute injury. However, due to the lack of treatment, more and more individuals with this condition enter a chronic state, to which very little research effort has been dedicated. SCI is a complex condition. It involves damage to axons, death of neurons, neuroinflammation, glial scar formation, loss of myelin, and lack of remyelination. It is clear that effective treatment will require combinatorial approaches. The 12 invited articles for this special issue on SCI provide an update on many of these areas of SCI research. Here, I highlight the articles and reviews by theme.Severe SCI involves severing of axons, breaking ascending and descending connections. Inhibitory molecules in the environment of the adult central nervous system, such as the myelin-associated inhibitors and proteoglycans in glial scars, were thought to be the major cause of the lack of regeneration for many years [1] .However, efforts to regenerate axons across a lesion site in the mammalian spinal cord by overcoming this inhibition have not been successful. In some cases, axon regeneration into cell grafts can be achieved, as in studies using preconditioning lesion paradigms of sensory axons [2] .But few axons project beyond the lesion and reach longrange targets. In recent years, more attention has been shifted to enhancing the intrinsic growth capacity of adult central nervous system axons. Deletion of pTEN (phosphatase and tensin homolog) induces unprecedented regeneration across the fully-transacted spinal cord [3] .Neurons derived from embryos or induced pluripotent stem cells that have strong intrinsic growth properties can ignore inhibitory cues in the adult spinal cord and grow long distances up and down the cord [4] . In partial injury, rerouting and sprouting of axons result in circuit reorganization in the spared tissue and have been shown to be effective in restoring function using a combination of pharmacological and electrophysiological stimulation and robot-assisted rehabilitation techniques [5,6] . Molecular mechanisms that promote or inhibit axon growth have been studied, using various injury paradigms, in different neuronal types and species. Some species have poor central regeneration, whereas others have the capacity to regenerate. Axons in the peripheral nervous system of mammals also show extensive regeneration. The review by Martin Oudega of the University of Pittsburgh [7] provides a comprehensive discussion comparing the molecular mechanisms found in mammals and zebrafish.These comparisons allow for a better understanding of the underlying principles. Remarkably, regeneration in the zebrafish central nervous system is also incomplete. Some axon tracts can regenerate but others cannot. This makes zebrafish an interesting model system for SCI research along with the ...

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Section: Sci Is a Complex Condition It Involves Damage Tomentioning

confidence: 99%

An update on spinal cord injury research

Zou

2013

Neurosci. Bull.

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“…Astrogliosis is a prominent feature of many diseases and injuries including Alzheimer disease, stroke, epilepsy, and traumatic brain and spinal cord injury (23)(24)(25). In response to a severe injury such as a spinal cord or traumatic brain injury, astrocytes become reactive and undergo a plethora of changes including cytoskeletal hypertrophy characterized by increased expression of glial fibrillary acidic protein and proliferation, and astrocytes begin to express many extracellular matrix molecules including chondroitin sulfate proteoglycans, laminins, and fibronectin (26). Together, these reactive astrocytes and the extracellular matrix form a dense glial scar that has both positive and negative consequences for nervous system repair.…”

Section: Astrocytesmentioning

confidence: 99%

Glial Contributions to Neural Function and Disease

Rasband

2016

Molecular & Cellular Proteomics

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The nervous system consists of neurons and glial cells. Neurons generate and propagate electrical and chemical signals, whereas glia function mainly to modulate neuron function and signaling. Just as there are many different kinds of neurons with different roles, there are also many types of glia that perform diverse functions. For example, glia make myelin; modulate synapse formation, function, and elimination; regulate blood flow and metabolism; and maintain ionic and water homeostasis to name only a few. Although proteomic approaches have been used extensively to understand neurons, the same cannot be said for glia. Importantly, like neurons, glial cells have unique protein compositions that reflect their diverse functions, and these compositions can change depending on activity or disease. Here, I discuss the major classes and functions of glial cells in the central and peripheral nervous systems.

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“…At the acute and subacute phases after SCI, the reactive astrocytes serve to separate the healthy tissue from the lesion area by restoring the blood-spinal cord barrier (75). This prevents the potential overwhelming inflammatory response (76), massive cellular degeneration and death (77), and tissue damage during the secondary injury (78). Therefore, a number scholars believe that astrogliosis after CNS injury is dependent on STAT3 activation, an indispensable step for the formation of glia scar and limitation of the spread of inflammation (70).…”

Section: Time-dependent Effects Of the Jak-stat Pathway In Reactive Amentioning

confidence: 99%

“…Reactive astrocytes can secrete and respond to a number of vital cytokines, which affects the cellular state of the surrounding cells (microglia and neurons) and of astrocytes themselves (82). Reactive astrocytes can preserve neurons and oligodendrocytes, and protect motor functions after SCI (72,76,78), potentially due to the astrocyte-secretory polypeptides (astrocyte-derived cytokines and trophic factors), which alter the microenvironment (83)(84)(85). These cytokines include IL-1β, TNF-α, IL-6, IL-11 and transforming growth factor-β1 (86)(87)(88)(89)(90)(91)(92) and the trophic factors include brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, nerve growth factor (NGF), CNTF, basic fibroblast growth factor and leukemia inhibiting factor (LIF) (93)(94)(95)(96)(97).…”

Section: Astrocyte-secretory Polypeptides Promote Neuroprotection Viamentioning

confidence: 99%

The role of the JAK-STAT pathway in neural stem cells, neural progenitor cells and reactive astrocytes after spinal cord injury

et al. 2014

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Abstract.Patients with spinal cord injuries can develop severe neurological damage and dysfunction, which is not only induced by primary but also by secondary injuries. As an evolutionarily conserved pathway of eukaryotes, the JAK-STAT pathway is associated with cell growth, survival, development and differentiation; activation of the JAK-STAT pathway has been previously reported in central nervous system injury. The JAK-STAT pathway is directly associated with neurogenesis and glia scar formation in the injury region. Following injury of the axon, the overexpression and activation of STAT3 is exhibited specifically in protecting neurons. To investigate the role of the JAK-STAT pathway in neuroprotection, we summarized the effect of JAK-STAT pathway in the following three sections: Firstly, the modulation of JAK-STAT pathway in proliferation and differentiation of neural stem cells and neural progenitor cells is discussed; secondly, the time-dependent effect of JAK-STAT pathway in reactive astrocytes to reveal their capability of neuroprotection is revealed and lastly, we focus on how the astrocyte-secretory polypeptides (astrocyte-derived cytokines and trophic factors) accomplish neuroprotection via the JAK-STAT pathway.

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The glial scar in spinal cord injury and repair

Cited by 166 publications

References 134 publications

An update on spinal cord injury research

An update on spinal cord injury research

Glial Contributions to Neural Function and Disease

The role of the JAK-STAT pathway in neural stem cells, neural progenitor cells and reactive astrocytes after spinal cord injury

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