Brain-derived and glial cell line-derived neurotrophic factors protect a catecholaminergic cell line from dopamine-induced cell death

Gong, Li; Wyatt, Richard Jed; Baker, Ivory; Masserano, Joseph M.

doi:10.1016/s0304-3940(99)00148-2

Cited by 41 publications

(20 citation statements)

References 18 publications

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“…Several neurotrophins have been shown to support dopaminergic neurons, including BDNF (Spina et al, 1992;Frim et al, 1994;Tsukahara et al, 1995), GDNF (Cheng et al, 1998;Date et al, 1998), FGF (Otto and Unsicker, 1994), and EGF (Hadjiconstantinou et al, 1991). Neurotrophins prevent cell death through a number of mechanisms including interference with intrinsic cell death programs (Schabitz et al, 2000;Heaton et al, 2003), as well as modulation of oxidative stress (Spina et al, 1992;Kirschner et al, 1996;Skaper et al, 1998;Gong et al, 1999;Petersen et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Glia cell number modulates sensitivity to MPTP in mice

Smeyne

Jiao

Shepherd

et al. 2005

Glia

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Free radical damage has been shown to play a significant role in the pathogenesis of a number of neurodegenerative diseases including Parkinson's disease. One model of experimental parkinsonism is the loss of substantia nigra cells following administration of MPTP. Previously, it has been shown that a number of inbred strains of mice have differential responses to this toxin, and this difference is dependent on glial cells. In this study, the number of glial cells in the substantia nigra pars compacta of C57Bl/6J (MPTP-sensitive) and Swiss Webster (MPTP-resistant) strains of mice was examined. The C57Bl/6J mice have an approximately 50% lower number of GFAP+ and S-100beta glial cells than the Swiss Webster mice. C57Bl/6J mice have a 25% increased number of resident nonactivated microglial cells. To determine whether this difference in cell number has functional significance, we used an in vitro SN culture system that allowed us to manipulate the number of glial cells. When C57Bl/6 neurons were grown on a glial mat plated with twice the number of cells, we were able to rescue the MPTP-sensitive neurons from toxin-induced cell death. This suggests that the number of glial cells in the SNpc may be an important factor in the survival of dopaminergic neurons following exposure to xenobiotics.

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Section: Introductionmentioning

confidence: 99%

Glia cell number modulates sensitivity to MPTP in mice

Smeyne

Jiao

Shepherd

et al. 2005

Glia

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“…Several neurotrophic factors have been reported to help rescue neurons and repair neuronal injury. These include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial-cell line-derived neurotrophic factor (GDNF), insulin-like growth factor, basic fibroblast growth factor (bFGF), transforming growth factor (TGF)-beta 3, neurotrophin-3 (NT-3), NT-4/5, and NT-6 (Gong et al 1999;Hyman et al 1994;Ikeda et al 2000;Krieglstein et al 1996;Zawada et al 1998). Although these neurotrophic factors are also known to be upregulated after hypoxia-ischemia in the neonatal rat (Ikeda et al 2002), this endogenous upregulation seems to be insufficient to support neural differentiation from progenitor cells.…”

Section: Exogenous Enrichment Of the Milieu Around The Injurymentioning

confidence: 99%

Stem cells and neonatal brain injury

Ikeda

2007

Cell Tissue Res

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Recent advances in regenerative medicine and in our understanding of neurogenesis may lead to new ways of recovering neuronal function lost or damaged during the perinatal period; such injuries are not amenable to conventional therapies. We review recent experimental studies based on immature rodental models of neonatal brain injury, especially hypoxic-ischemic encephalopathy. The developing brain is revealed to have considerable potential with respect to proliferation and migration to the injured site. However, the generation of fully differentiated neurons is extremely limited after brain injuries. Aggressive efforts to adjust the environment of the damaged brain in which tissue regeneration is occurring or more cautious stem cell transplantation will be required for the successful treatment of developmental brain injury.

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“…Furthermore, the induction of cyclooxygenase-2 (COX-2) within the dopaminergic neurons after MPTP injection (42,81) can also serve as a source of ROS. pounds.…”

Section: Chmentioning

confidence: 99%

“…s [42,66,111,140,145] as well as interference with the MPTP, which is structurally similar to a number of rigidity, For reasons that wve do not know, the dopamiine nonakinesia./bradykinesia and postural instability, these are ron seents to be miore vulnerable to damage than mainly, thou-g'h not exclusively, the dopaniincrgie net[-any other neuron in the brain. Althoughi hypotheses rons in the SUbstantia nigra pars compacta (SNpc) of damage to the dopamaine neuron include oxidnwhose fibres p~roject to the corpus striatumn.…”

Section: Ri Sineyne V Jackvon-lewis / Molecular Brain Research 134 mentioning

confidence: 99%

Role of Inflammation in MPTP-Induced Dopaminergic Degeneration

Przedborski¹

2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of Information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302 Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. se. TASK NUMBER 5f. WORK UNIT NUMBER REPORT DATE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERColumbia University New York, NY 10032 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTESOriginal contains colored plates: ALL DTIC reproductions will be in black and white. ABSTRACTWe are investigating the role of inflammation in the death of the dopamine (DA) neuron in the substantia nigra of MPTPtreated mice. Studies in our model over the course of this program project show that microglia are the source of superoxide and nitric oxide through up-regulation of the microglial enzymes NADPH oxidase and inducible nitric oxide synthase (iNOS). We show that activation of microglia in vivo occurs as early as 24 hours after MPTP administration at which time the presence of superoxide in the SNpc after MPTP is noted using hydroethidium histochemistry. M40401, a nonpeptidyl SOD mimetic with catalytic activity equal to or greater than native MnSOD decreased the presence of superoxide and attenuated microglial activation in the SNpc of our mice. Minocycline, a second generation antibiotic, inhibited iNOS up-regulation and also reduced microglial activation. Further, we demonstrate that cyclooxygenase-2 is a part of the inflammatory response in MPTP-treated mice. Our neuronal/microglial cultures now that they are up and running, should give a more exact timeframe of microglial activation in relation to DA neuron death in the MPTP mouse model of PD. Furthermore, we identify components of microglia that may be therapeutic targets. Parkinson's disease (PD) is a common neurodegenerative disorder characterized behaviorally by resting tremor, rigidity, akinesialbradykinesia and postural instability (Fahn and Przedborski, 2000). Neurons associated with the behavioral component of PD are mainly, though not exclusively, the dopaminergic (DA) ...

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Brain-derived and glial cell line-derived neurotrophic factors protect a catecholaminergic cell line from dopamine-induced cell death

Cited by 41 publications

References 18 publications

Glia cell number modulates sensitivity to MPTP in mice

Glia cell number modulates sensitivity to MPTP in mice

Stem cells and neonatal brain injury

Role of Inflammation in MPTP-Induced Dopaminergic Degeneration

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