Astrocytes Are the Major Source of Nerve Growth Factor Upregulation Following Traumatic Brain Injury in the Rat

Goss, James R.; O’Malley, Michael J.; Zou, Lanling; Styren, Scot; Kochanek, Patrick M.; DeKosky, Steven T.

doi:10.1006/exnr.1997.6712

Cited by 147 publications

(90 citation statements)

References 52 publications

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“…Specifically, reactive astrogliosis is denoted by increased immunoreactivity of glial fibrillary acid protein (GFAP), which is a distinct cellular marker of astrocytes. 14,48,[71][72][73][74]111 It has been demonstrated that reactive adult astrocytes upregulate the production of laminin and neurotrophin C. 75,76 In addition to the endogenously present myelinassociated neurite growth inhibitory constitutents, reactive astrocytes form an astroglial scar that acts as a physical and/or chemical barrier to axonal regeneration. 8,35,72,77,78 Proximity to the lesion epicentre determines whether the reactive glial environment will be growth supportive or inhibitory.…”

Section: Experimental Modelsmentioning

confidence: 99%

Post-traumatic inflammation following spinal cord injury

2003

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Section: Experimental Modelsmentioning

confidence: 99%

Post-traumatic inflammation following spinal cord injury

2003

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“…Reactive glia has been shown to secrete neurotrophic factors in response to various stimuli (Ridet et al 1997;Yoshida and Toya 1997, Toyomoto, 2004#49, Aschner, 1998 In particular, astrocytes were shown to up-regulate synthesis of NGF following treatment with LPS (Galve-Roperh et al 1997;Xiong et al 1999), glutamate (Wu et al 2004) and nitric oxide donors, such as SIN1 and peroxynitrite (Tanaka et al 1999;Cassina et al 2001), and also after injury (Yu et al 1996;Goss et al 1998;Micera et al 1998;Krenz and Weaver 2000). Recently, induction of proNGF in vivo was shown in GFAP-positive cells within the basal forebrain following kainic acid seizures {Volosin, 2006 #127}.…”

Section: Pro-neurotrophins Production By Astrocytesmentioning

confidence: 99%

Pro-NGF secreted by astrocytes promotes motor neuron cell death

Domeniconi

Hempstead

Chao

2007

Molecular and Cellular Neuroscience

109

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It is well established that motor neurons depend for their survival on many trophic factors. In this study, we show that the precursor form of NGF (proNGF) can induce the death of motor neurons via engagement of the p75 neurotrophin receptor. The pro-apoptotic activity was dependent upon the presence of sortilin, a p75 co-receptor expressed on motor neurons. One potential source of proNGF is reactive astrocytes, which upregulate the levels of proNGF in response to peroxynitrite, an oxidant and producer of free radicals. Indeed, motor neuron viability was sensitive to conditioned media from cultured astrocytes treated with peroxynitrite and this effect could be reversed using a specific antibody against the pro-domain of proNGF. These results are consistent with a role for activated astrocytes and proNGF in the induction of motor neuron death and suggest a possible therapeutic target for the treatment of motor neuron disease.

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“…Transplantation of astrocytes may be beneficial because they are a major source of nerve growth factor following TBI [9]. It has also been shown that GDNF is neuroprotective and is released by astrocytes [15].…”

Section: Introductionmentioning

confidence: 99%

Transplantation of GABAergic neurons but not astrocytes induces recovery of sensorimotor function in the traumatically injured brain

Becerra

Tatko

Pak

et al. 2007

Behavioural Brain Research

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Embryonic stem (ES) cells have been investigated in many animal models of injury and disease. However, few studies have examined the ability of pre-differentiated ES cells to improve functional outcome following traumatic brain injury (TBI). The purpose of the present study was to compare the effect of murine ES cells that were pre-differentiated into GABAergic neurons or astrocytes on functional recovery following TBI. Neural and astrocyte induction was achieved by co-culturing ES cells on a bone marrow stromal fibroblast (M2-10B4) feeder layer and incubating them with various mitogenic factors. Rats were initially prepared with a unilateral controlled cortical contusion injury of the sensorimotor cortex or sham procedure. Rats were transplanted 7 days following injury with ∼100K GABAergic neurons, astrocytes, fibroblasts, or media. Animals were assessed on a battery of sensorimotor tasks following transplantation. The stromal fibroblast cells (M2-10B4), as a control cell line, did not differ significantly from media infusions. Transplantation of GABAergic neurons facilitated complete and total recovery on the vibrissae-forelimb placing test as opposed to all other groups, which failed to show any recovery. It was also found that GABAergic neurons reduced the magnitude of the initial impairment on the limb use test. Histological analysis revealed infiltration of host brain with transplanted neurons and astrocytes. The results of the present study suggest that transplantation of pre-differentiated GABAergic neurons significantly induces recovery of sensorimotor function; whereas, astrocytes do not.

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Astrocytes Are the Major Source of Nerve Growth Factor Upregulation Following Traumatic Brain Injury in the Rat

Cited by 147 publications

References 52 publications

Post-traumatic inflammation following spinal cord injury

Post-traumatic inflammation following spinal cord injury

Pro-NGF secreted by astrocytes promotes motor neuron cell death

Transplantation of GABAergic neurons but not astrocytes induces recovery of sensorimotor function in the traumatically injured brain

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