The S100B Protein and Traumatic Brain Injury

Cotena, Simona; Piazza, Ornella; Storti, M.

doi:10.3171/ped.2006.104.6.435

Cited by 6 publications

(3 citation statements)

References 5 publications

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“…In the brain, S100B, a member of the S100 superfamily of calcium binding proteins, is produced by astroglial cells and specifically released into the neuropil in response to a number of neurochemical factors including serotonin (Whitaker‐Azmitia et al, 1989, 1990) tissue insults or trauma (Anderson et al, 2001; Cotena et al, 2006) and ischemia (Parker et al, 1998; Rothermundt et al, 2003) and decreased release by glutamate (Tramontina et al, 2006). Although predominantly expressed by astroglia, S100B can also be expressed at much lower levels in microglia (Adami et al, 2001), radial glia (Castagna et al, 2003), and oligodendrocytes (Richter‐Landsberg and Heinrich, 1995).…”

Section: Discussionmentioning

confidence: 99%

Vitamin E increases S100B‐mediated microglial activation in an S100B‐overexpressing mouse model of pathological aging

Bialowas‐McGoey

Lesicka

Whitaker‐Azmitia

2008

Glia

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S100B is a calcium-binding protein released by astroglial cells of the brain capable of producing numerous extracellular effects. Although the direct molecular mechanism remains unknown, these effects can be trophic including differentiation, growth, recovery, and survival of neurons when the S100B protein is mainly oxidized and neurotoxic including apoptosis and neuroinflammatory processes marked by microglial activation when in a reduced state. S100B and its receptor RAGE (receptor for advanced glycation end products) have been found to be increased in Alzheimer's disease, Down syndrome, with tissue trauma and ischemia. In the current study, we examined the binding of the S100B receptor (RAGE) on microglial cells and the developmental effects of the antioxidant vitamin E on microglial activation and the upregulation of RAGE in an S100B over-expressing mouse model of pathological aging. We report that RAGE is co-localized on activated microglial cells and vitamin E induced dramatic increases in microglial activation as well as total microglial relative optical density that was accompanied by upregulation of the RAGE receptor, particularly in the CA1 region of the hippocampus. Our findings suggest further investigation into the potential role of vitamin E in reducing the oxidation state of the S100B protein and its influence on neuroinflammatory processes marked by microglial activation in vivo.

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Section: Discussionmentioning

confidence: 99%

Vitamin E increases S100B‐mediated microglial activation in an S100B‐overexpressing mouse model of pathological aging

Bialowas‐McGoey

Lesicka

Whitaker‐Azmitia

2008

Glia

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“…1365-2133.2006.07746.x SIR, Epidermolysis bullosa acquisita (EBA) is an acquired autoimmune bullous disease of the skin and mucous membranes characterized by IgG autoantibodies to type VII collagen, the main constituent of the anchoring fibrils of the dermalepidermal juction. 1,2 Inflammatory bowel diseases (IBD) may be associated with autoimmunity to type VII collagen. 3,4 Erythema gyratum repens (EGR), an obligate paraneoplastic syndrome, may occur in patients with pemphigoid diseases.…”

Section: Hours After Irradiationmentioning

confidence: 99%

“…Among these protein isoforms, the S100 β protein is found predominantly in cells of the central nervous system, Langerhans cells and melanocytes. It has been proven to be of clinical use in indicating brain damage 2 after trauma or ischaemia, and has also been proposed as a marker for different skin disorders 3,4 . The most established application of S100 β is as a serum tumour marker with prognostic value for the course of malignant melanoma, indicating macrometastasis but not micrometastasis 5,6 .…”

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confidence: 99%