Evidence for a wide extra-astrocytic distribution of S100B in human brain

Steiner, Johann; Bernstein, Hans‐Gert; Bielau, Hendrik; Berndt, Annika; Brisch, Ralf; Mawrin, Christian; Keilhoff, Gerburg; Bogerts, Bernhard

doi:10.1186/1471-2202-8-2

Cited by 225 publications

(149 citation statements)

References 50 publications

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“…Therefore, the measurement of these proteins might potentially be useful as specific biomarker of IS (Table 1). Among them, the release of calcium-binding proteins S100B has been traditionally ascribed to astrocyte dysfunction, but recent studies rather indicate a role as a marker of BBB injury [188,189]. Serum levels of S100B increase at 8–10 h from symptom onset, reach the peak after 72 h and then drop in levels at 96 h [146].…”

Section: Inflammatory Mediators As Potential Diagnostic or Prognosmentioning

confidence: 99%

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

Bonaventura

Liberale

Vecchiè

et al. 2016

IJMS

133

114

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After an acute ischemic stroke (AIS), inflammatory processes are able to concomitantly induce both beneficial and detrimental effects. In this narrative review, we updated evidence on the inflammatory pathways and mediators that are investigated as promising therapeutic targets. We searched for papers on PubMed and MEDLINE up to August 2016. The terms searched alone or in combination were: ischemic stroke, inflammation, oxidative stress, ischemia reperfusion, innate immunity, adaptive immunity, autoimmunity. Inflammation in AIS is characterized by a storm of cytokines, chemokines, and Damage-Associated Molecular Patterns (DAMPs) released by several cells contributing to exacerbate the tissue injury both in the acute and reparative phases. Interestingly, many biomarkers have been studied, but none of these reflected the complexity of systemic immune response. Reperfusion therapies showed a good efficacy in the recovery after an AIS. New therapies appear promising both in pre-clinical and clinical studies, but still need more detailed studies to be translated in the ordinary clinical practice. In spite of clinical progresses, no beneficial long-term interventions targeting inflammation are currently available. Our knowledge about cells, biomarkers, and inflammatory markers is growing and is hoped to better evaluate the impact of new treatments, such as monoclonal antibodies and cell-based therapies.

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Section: Inflammatory Mediators As Potential Diagnostic or Prognosmentioning

confidence: 99%

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

Bonaventura

Liberale

Vecchiè

et al. 2016

IJMS

133

114

View full text Add to dashboard Cite

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“…S100β is highly expressed in the human brain, including prominent expression in astrocytes and in many neural cell types [107]. The physiological release of S100β exerts neurotrophic effects in the brain [94] and intense S100β expression also is observed within white matter tracts, including the corpus callosum [108].…”

Section: Damage Associated Molecular Patterns (Damps): Mediators Omentioning

confidence: 99%

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Braun

Vaibhav

Saad

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

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“…S100B is a glia-derived neurotrophic marker and an acidic and calcium-binding protein that is primarily produced by astrocytes and oligodendrocytes in the human brain [6]. Astrocytes are the main type of glial cells and are distributed throughout the nervous system.…”

Section: Introductionmentioning

confidence: 99%

Venlafaxine ameliorates the depression-like behaviors and hippocampal S100B expression in a rat depression model

Wang

Zhang

et al. 2016

Behav Brain Funct

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BackgroundAccumulating evidence has indicated that S100B may be involved in the pathophysiology of depression. No published study has examined the effect of the antidepressant drug venlafaxine on S100B in animal models of depression. This study investigated S100B expression in the hippocampus and assessed the effect of venlafaxine on S100B mRNA level and protein expression in rats exposed to chronic unpredictable mild stress (CUMS).MethodsForty Sprague-Dawley rats were randomly divided into four groups as control, 0, 5 and 10 mg venlafaxine groups. The venlafaxine groups were exposed to CUMS from day 2 to day 43. Venlafaxine 0, 5 and 10 mg/kg were then administered from day 23 to day 43. We performed behavioral assessments with weight change, open-field and sucrose preference, and analyzed S100B protein expression and mRNA level in the hippocampus.ResultsThe CUMS led to a decrease in body weight, locomotor activity and sucrose consumption, but venlafaxine treatment (10 mg) reversed these CUMS-induced decreases Also, CUMS increased S100B protein expression and mRNA level in the hippocampus, but venlafaxine treatment (10 mg) significantly decreased S100B protein expression and mRNA level, which were significantly lower than the other treatment groups, without significant difference between the 10 mg venlafaxine and the control groups.ConclusionsOur findings showed that venlafaxine treatment (10 mg) may improve the depression-like behaviors and decrease over-expression of S100B protein and mRNA in the hippocampus in a rat model of depression.Electronic supplementary materialThe online version of this article (doi:10.1186/s12993-016-0116-x) contains supplementary material, which is available to authorized users.

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Evidence for a wide extra-astrocytic distribution of S100B in human brain

Cited by 225 publications

References 50 publications

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

Update on Inflammatory Biomarkers and Treatments in Ischemic Stroke

White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Venlafaxine ameliorates the depression-like behaviors and hippocampal S100B expression in a rat depression model

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