Neurotrophic protein S100 beta stimulates glial cell proliferation.

Selinfreund, R.; Barger, Steven W.; Pledger, W. J.; Eldik, Linda J. Van

doi:10.1073/pnas.88.9.3554

Cited by 297 publications

(185 citation statements)

References 58 publications

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“…Several previous reports suggested that the S100B protein functions as a trophic factor (17)(18)(19). However, mice completely lacking S100B developed normally and there was no detectable abnormality in histological architecture of the mutant brain.…”

Section: Discussionmentioning

confidence: 92%

“…Mutant mice reached sexual maturity and both male and female mice were fertile. Despite several lines of evidences suggesting that S100B has trophic activity for glia and neurons (17)(18)(19), no anatomical abnormalities were observed in mutant brains (data not shown). We observed no abnormalities in their home cage behavior for up to 18 months of age.…”

Section: S100b-null Mice Developedmentioning

confidence: 88%

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Glial protein S100B modulates long-term neuronal synaptic plasticity

Nishiyama

Knöpfel

Endo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

243

168

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Glial cells are traditionally regarded as elements for structural support and ionic homeostasis, but have recently attracted attention as putative integral elements of the machinery involved in synaptic transmission and plasticity. Here, we demonstrate that calcium-binding protein S100B, which is synthesized in considerable amounts in astrocytes (a major glial cell subtype), modulates long-term synaptic plasticity. Mutant mice devoid of S100B developed normally and had no detectable abnormalities in the cytoarchitecture of the brain. These mutant mice, however, had strengthened synaptic plasticity as identified by enhanced longterm potentiation (LTP) in the hippocampal CA1 region. Perfusion of hippocampal slices with recombinant S100B proteins reversed the levels of LTP in the mutant slices to those of the wild-type slices, indicating that S100B might act extracellularly. In addition to enhanced LTP, mutant mice had enhanced spatial memory in the Morris water maze test and enhanced fear memory in the contextual fear conditioning. The results indicate that S100B is a glial modulator of neuronal synaptic plasticity and strengthen the notion that glial-neuronal interaction is important for information processing in the brain.S everal lines of evidence suggest that glial cells play an active role in excitatory neurotransmission in the central nervous system (1, 2). For instance, astrocytes can release glutamate in response to physiological increases in their intracellular calcium concentration, and then evoke substantial glutamatergic currents in neighboring neurons (3). Oligodendrocyte precursor cells directly receive glutamatergic inputs from hippocampal pyramidal neurons (4). These findings, together with earlier studies showing that glial cells express many types of neurotransmitter receptors and respond to neurotransmitter by generating slowly propagating calcium waves (5), suggest that glialneuronal reciprocal signaling may play a role in synaptic plasticity and eventually in information processing in the brain. Indeed, this notion has been supported by the findings that the mice devoid of glial fibrillary acidic protein (GFAP: an intermediate filament specific to astrocytes) showed enhanced longterm potentiation (LTP) in the hippocampal CA1 region and decreased long-term depression in the cerebellum associated with impaired eye-blink conditioning (6, 7). However, the molecular mechanism underlying glial-neuronal interactions is poorly understood.One of the candidates that might be involved in glia-to-neuron signaling is the calcium-binding protein S100B. S100B is a member of the S100 family of proteins containing two EF-handtype calcium-binding domains (8). The highest level of expression of the S100B protein is in the brain and is found primarily in the cytoplasm of astrocytes (9). Results of in vitro studies suggest a variety of intracellular functions of S100B, including cell growth, cell structure, energy metabolism, and calcium homeostasis (8). S100B is secreted from astrocytes, suggesting that it might ...

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Section: Discussionmentioning

confidence: 92%

Section: S100b-null Mice Developedmentioning

confidence: 88%

Glial protein S100B modulates long-term neuronal synaptic plasticity

Nishiyama

Knöpfel

Endo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

243

168

View full text Add to dashboard Cite

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“…The present results suggest that S100A1, but not S100A4, produced by the tumour cells could stimulate muscle proliferation and there are several possible explanations for this effect. However, the previously reported extracellular activity of some S100 proteins, notably the neuronal S100B, which is neurotrophic for cultured glial cells and astrocytes (Selinfreund et al, 1991), raises the possibility that S100A1 might exert its effect extracellularly on host muscle cells in vivo.…”

Section: (T) Invading Muscle Cells (M) (C) Primary Tumour Of Rama 37mentioning

confidence: 87%

Mutually antagonistic actions of S100A4 and S100A1 on normal and metastatic phenotypes

et al. 2004

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Increased levels of the homodimeric calcium-binding protein, S100A4, have been shown to cause a metastatic phenotype in at least three independent model systems of breast cancer and its presence in carcinoma cells has been shown to be associated with a reduction in the survival of patients suffering from a range of different cancers. S100A4 has been shown to interact in vitro with another member of the S100 family of proteins, S100A1. The purpose of the present study was to find out whether S100A1 could affect S100A4 function. Fluorescence resonance energy transfer was used to show the interaction of S100A4 and S100A1 in living cells and the binding affinities between S100A4 and S100A1 were determined using a biosensor. S100A1 reduced the S100A4 inhibition of nonmuscle myosin A self-association and phosphorylation in vitro. S100A1 reduced S100A4 induced motility and growth in soft agar and metastasis in vivo. The results show for the first time that interactions between different S100 proteins can affect cancer-related activity, and that the presence of S100A1 protein in carcinoma cells might modulate the effect of S100A4 on their metastatic abilities.

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“…Moreover, the increased S100ß and FGF-2 in reactive satellite cells of axotomized DRG and lesioned sciatic nerve may also be associated with local neovascularization, gliogenesis and repair 34 as well as to paracrine neuronal trophism and plasticity in remaining DRG peripheral motor neurons.…”

Section: Discussionmentioning

confidence: 99%

S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury

et al. 2008

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PURPOSE: The neurotrophic factor fibroblast growth factor-2 (FGF-2, bFGF) and Ca++ binding protein S100ß are expressed by the Schwann cells of the peripheral nerves and by the satellite cells of the dorsal root ganglia (DRG). Recent studies have pointed out the importance of the molecules in the paracrine mechanisms related to neuronal maintenance and plasticity of lesioned motor and sensory peripheral neurons. Moreover, cultured Schwann cells have been employed experimentally in the treatment of central nervous system lesions, in special the spinal cord injury, a procedure that triggers an enhanced sensorymotor function. Those cells have been proposed to repair long gap nerve injury. METHODS: Here we used double labeling immunohistochemistry and Western blot to better characterize in vitro and in vivo the presence of the proteins in the Schwann cells and in the satellite cells of the DRG as well as their regulation in those cells after a crush of the rat sciatic nerve. RESULTS: FGF-2 and S100ß are present in the Schwann cells of the sciatic nerve and in the satellite cells of the DRG. S100ß positive satellite cells showed increased size of the axotomized DRG and possessed elevated amount of FGF-2 immunoreactivity. Reactive satellite cells with increased FGF-2 labeling formed a ring-like structure surrounding DRG neuronal cell bodies.Reactive S100ß positive Schwann cells of proximal stump of axotomized sciatic nerve also expressed higher amounts of FGF-2. CONCLUSION: Reactive peripheral glial cells synthesizing FGF-2 and S100ß may be important in wound repair and restorative events in the lesioned peripheral nerves.

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Neurotrophic protein S100 beta stimulates glial cell proliferation.

Cited by 297 publications

References 58 publications

Glial protein S100B modulates long-term neuronal synaptic plasticity

Glial protein S100B modulates long-term neuronal synaptic plasticity

Mutually antagonistic actions of S100A4 and S100A1 on normal and metastatic phenotypes

S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury

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