Differential effects of SOCS2 on neuronal differentiation and morphology

Scott, Hannah; Stebbing, Margaret Susanne; Walters, Claire E.; McLenachan, Samuel; Ransome, Mark I.; Nichols, Nancy R.; Turnley, Ann M.

doi:10.1016/j.brainres.2005.10.032

Cited by 39 publications

(32 citation statements)

References 22 publications

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“…Excess medium and non-adherent cells were then removed by gentle aspiration and control media or media containing mouse GH (National Hormone Pituitary Program, Riverside, CA, USA) at 10 -6 or 10 -9 M were applied to the coverslips. These doses of GH are in the physiological range and comparable to those used by Turnley (2005), Scott et al (2006) and Byts et al (2008), but far lower than those used by Lyuh et al (2007). Cells on the coverslips were then incubated for 72 h with changes in the media every 24 h. After incubation, the cells were fixed in 4% (w/v) paraformaldehyde for 15 min, then washed with PBS.…”

Section: Immunohistochemistrymentioning

confidence: 75%

“…This is in agreement with the ability of human GH to promote neurite development in primary neuronal cultures of the fetal mouse hippocampus (Byts et al 2008) and in hybrid cells derived from both N18TG2 neuroblastoma cells and cells from the rat ventral spinal cord (Lyuh et al 2007). This finding is, however, in contrast with the reported inability of rat GH to induce neurite development in fetal mouse neural progenitor cells (Turnley et al 2002;Scott et al 2006). The reason for this discrepancy is unclear, especially as GHRs in cultures of fetal rat cerebral cortical neurons have far greater affinity for rodent GH than non-rodent GH (Moderscheim et al 2007).…”

Section: Discussionmentioning

confidence: 92%

“…Turnley has asserted that GH inhibits neurite outgrowth from neural progenitor cells (Turnley et al 2002;Turnley 2005;Scott et al 2006), but Byts et al (2008) recently found that GH promoted neurite development in the same fetal hippocampal cells. This view is supported by Lyuh et al (2007), who found that GH induced the production of neurite outgrowths from cultured neuronal hybrid cells.…”

Section: Introductionmentioning

confidence: 99%

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Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

et al. 2009

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Neuroblastoma cells are undifferentiated cells derived from the neural crest and are commonly used as models for studying neural function. Mouse N1E-115 neuroblastoma cells are derived from cancerous tissue and provide a model for studying the oncogenesis of neural cells. As growth hormone (GH) has been implicated as an autocrine or paracrine involved in neural regulation and in the induction or progression of cancer, the possibility that N1E-115 cells are sites of GH production and GH action was assessed. Using RT-PCR, cultured N1E-115 cells were found to express the mouse GH and GH receptor (GHR) genes. Immunocytochemistry demonstrated that both of the translated proteins (GH and its receptor) were abundantly present in the cytoplasm of these cells and their co-localization was established by confocal cytochemistry. GH action in these cells was determined in cells cultured for 72 h in the presence or absence of 10(-6) M or 10(-9) M mouse GH, which induced neurite sprouting and increased axon growth. In summary, the expression of GH and its receptor in GH responsive tumor-derived N1E-115 neuroblastoma cells suggests they provide a useful experimental model to assess GH actions in neural function or neural oncogenesis.

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Section: Immunohistochemistrymentioning

confidence: 75%

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

et al. 2009

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“…In-vitro, neural stem cells from SOCS2 -/-mice show a marked reduction in the number of neurons generated [171], as opposed to SOCS2Tg mice which show an increase in neuron number [172][173][174]. Additionally, PC12 cells and neural cells from SOCS2Tg mice demonstrate increased neurite outgrowth in tissue culture [171,[174][175][176].…”

Section: Socs2 In the Brainmentioning

confidence: 99%

“…Additionally, PC12 cells and neural cells from SOCS2Tg mice demonstrate increased neurite outgrowth in tissue culture [171,[174][175][176]. GH is an inhibitor of neural differentiation and its negative regulation by SOCS2 is evident by the reduction in neuronal differentiation in neural stem cell cultures of SOCS2 -/-mice [171,174].…”

Section: Socs2 In the Brainmentioning

confidence: 99%

Regulation of Basal and Injury-Induced Fate Decisions of Adult Neural Precursor Cells: Focus on SOCS2 and Related Signalling Pathways

Basrai¹,

Christie²,

Turnley³

2013

Trends in Cell Signaling Pathways in Neuronal Fate Decision

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Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome

Kaminen‐Ahola

Ahola

Flatscher-Bader

et al. 2010

Birth Defects Research

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Growth restriction, craniofacial dysmorphology, and central nervous system defects are the main diagnostic features of fetal alcohol syndrome. Studies in humans and mice have reported that the growth restriction can be prenatal or postnatal, but the underlying mechanisms remain unknown.We recently described a mouse model of moderate gestational ethanol exposure that produces measurable phenotypes in line with fetal alcohol syndrome (e.g., craniofacial changes and growth restriction in adolescent mice). In this study, we characterize in detail the growth restriction phenotype by measuring body weight at gestational day 16.5, cross-fostering from birth to weaning, and by extending our observations into adulthood. Furthermore, in an attempt to unravel the molecular events contributing to the growth phenotype, we have compared gene expression patterns in the liver and kidney of nonfostered, ethanol-exposed and control mice at postnatal day 28.We find that the ethanol-induced growth phenotype is not detectable prior to birth, but is present at weaning, even in mice that have been cross-fostered to unexposed dams. This finding suggests a postnatal growth restriction phenotype that is not due to deficient postpartum care by dams that drank ethanol, but rather a physiologic result of ethanol exposure in utero. We also find that, despite some catch-up growth after 5 weeks of age, the effect extends into adulthood, which is consistent with longitudinal studies in humans.Genome-wide gene expression analysis revealed interesting ethanol-induced changes in the liver, including genes involved in the metabolism of exogenous and endogenous compounds, iron homeostasis, and lipid metabolism.

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Differential effects of SOCS2 on neuronal differentiation and morphology

Cited by 39 publications

References 22 publications

Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

Regulation of Basal and Injury-Induced Fate Decisions of Adult Neural Precursor Cells: Focus on SOCS2 and Related Signalling Pathways

Postnatal growth restriction and gene expression changes in a mouse model of fetal alcohol syndrome

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