Differentiation of Mesencephalic Progenitor Cells into Dopaminergic Neurons by Cytokines

Ling, Zaodung; Potter, Elizabeth D.; Lipton, Jack W.; Carvey, Paul M.

doi:10.1006/exnr.1998.6715

Cited by 274 publications

(170 citation statements)

References 75 publications

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“…17 Angiogenic effects of rHuEPO have also been demonstrated on rat cardiomyocytes 19 and aortic tissue. 30 EPO and other hematopoietic cytokines may regulate the differentiation of neurons in the brain, 31 and a neurotrophic role of EPO has been postulated. 21,23,26,[32][33][34] EPO-R have been identified in the hippocampus, amygdala, and temporal cortex of the human brain, where endogenous EPO production by astrocytes is induced in an oxygen-dependent manner and may have a neuroprotective function.…”

Section: Discussionmentioning

confidence: 99%

Neurodevelopmental Outcome of Prematurely Born Children Treated With Recombinant Human Erythropoietin in Infancy

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Neurodevelopmental Outcome of Prematurely Born Children Treated With Recombinant Human Erythropoietin in Infancy

et al. 1999

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“…Second, experimentation in animals has confirmed that, in the absence of a specific pathogen, prenatal exposure to cytokine-releasing agents (Shi et al, 2003;Zuckerman et al, 2003;Zuckerman and Weiner, 2005;Meyer et al, 2005Meyer et al, , 2006aOzawa et al, 2006) is sufficient to induce psychopathology in later life. Third, in addition to their immunological roles (Curfs et al, 1997), pro-inflammatory cytokines have various neurodevelopmental effects (eg Ling et al, 1998;Jarskog et al, 1997;Gilmore et al, 2004). Hence, an imbalance in pro-inflammatory cytokine may trigger mal-neurodevelopment in the developing fetus and ultimately precipitate neuropathology and psychopathology in the adult offspring.…”

Section: Introductionmentioning

confidence: 99%

Relative Prenatal and Postnatal Maternal Contributions to Schizophrenia-Related Neurochemical Dysfunction after In Utero Immune Challenge

Meyer

Nyffeler

Schwendener

et al. 2007

Neuropsychopharmacol

197

193

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Prenatal exposure to infections represents a risk factor for the emergence of neuropsychiatric disorders in later life, including schizophrenia and autism. However, it remains essentially unknown whether this association is primarily attributable to prenatal and/or postnatal maternal effects on the offspring. Here, we addressed this issue by dissecting the relative contributions of prenatal inflammatory events and postnatal maternal factors in an animal model of prenatal viral-like infection. Pregnant mice were exposed to the inflammatory agent polyriboinosinic-polyribocytidilic acid (PolyI:C; 5 mg/kg, i.v.) or vehicle treatment on gestation day 9, and offspring born to PolyI:Cand vehicle-treated dams were cross fostered to surrogate rearing mothers that had either experienced inflammatory or sham treatment during pregnancy. We demonstrate that a variety of dopamine-and glutamate-related pharmacological and neuroanatomical disturbances emerge after prenatal immune challenge regardless of whether neonates were raised by vehicle-or PolyI:C-exposed surrogate mothers. However, the adoption of prenatal control animals to immune-challenged surrogate mothers was also sufficient to induce specific pharmacological and neuroanatomical abnormalities in the fostered offspring. Multiple schizophrenia-related dysfunctions emerging after prenatal immune challenge are thus mediated by prenatal but not postnatal maternal effects on the offspring, but immunological stress during pregnancy may affect postpartum maternal factors in such a way that being reared by an immune-challenged surrogate mother can confer risk for distinct forms of psychopathology in adult life.

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“…9 More specifically, it has been suggested that activation of pro-inflammatory cytokines, including interleukin (IL)-1b, IL-6 and tumor necrosis factor (TNF)-a, mediate the neurodevelopmental effects of maternal infections on the offspring. This class of cytokines can modulate neuronal differentiation, 10 survival 11 and dendrite growth and complexity in vitro. 12 They may also be critically involved in the precipitation of the long-term behavioral, cognitive and pharmacological consequences of prenatal immune challenge as shown in vivo.…”

Section: Introductionmentioning

confidence: 99%

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

et al. 2007

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Maternal infections during pregnancy increase the risk for schizophrenia and related disorders of putative neurodevelopmental origin in the offspring. This association has been attributed to enhanced expression of pro-inflammatory cytokines in the fetal environment in response to maternal immunological stimulation. In contrast, the specific roles of anti-inflammatory cytokines are virtually unknown in this context. Here, we demonstrate that genetically enforced expression of the anti-inflammatory cytokine interleukin (IL)-10 by macrophages attenuates the long-term behavioral and pharmacological consequences of prenatal immune activation in a mouse model of prenatal viral-like infection by polyriboinosinic-polyribocytidilic acid (PolyI:C; 2 mg/kg, intravenously). In the absence of a discrete prenatal inflammatory stimulus, however, enhanced levels of IL-10 at the maternal-fetal interface by itself also precipitates specific behavioral abnormalities in the grown offspring. This highlights that in addition to the disruptive effects of excess pro-inflammatory molecules, a shift toward enhanced antiinflammatory signaling in prenatal life can similarly affect cognitive and behavioral development. Hence, shifts of the balance between pro-and anti-inflammatory cytokine classes may be a critical determinant of the final impact on neurodevelopment following early life infection or innate immune imbalances.

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Differentiation of Mesencephalic Progenitor Cells into Dopaminergic Neurons by Cytokines

Cited by 274 publications

References 75 publications

Neurodevelopmental Outcome of Prematurely Born Children Treated With Recombinant Human Erythropoietin in Infancy

Neurodevelopmental Outcome of Prematurely Born Children Treated With Recombinant Human Erythropoietin in Infancy

Relative Prenatal and Postnatal Maternal Contributions to Schizophrenia-Related Neurochemical Dysfunction after In Utero Immune Challenge

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

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