Active secretion of S100B from astrocytes during metabolic stress

Gerlach, Rüdiger; Demel, G.; König, Hans-Georg; Groß, U.; Prehn, Jochen H.M.; Raabe, Andreas; Seifert, Volker; Kögel, Donat

doi:10.1016/j.neuroscience.2006.05.008

Cited by 114 publications

(84 citation statements)

References 15 publications

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“…18 The S100B protein is thought to function as a neurotrophic cytokine, conferring neuroprotective effects at lower levels of concentration. It may share function with p11 (S100A10), a molecule with a demonstrated reduction in both depressed patients and an animal model of depression which interacts with the serotonin 1B receptor.…”

Section: Discussionmentioning

confidence: 99%

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

et al. 2007

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The prefrontal cortex is believed to play a major role in depression and suicidal behavior through regulation of cognition, memory, recognition of emotion, and anxiety-like states, with numerous post-mortem studies documenting a prefrontal serotonergic dysregulation considered to be characteristic of depressive psychopathology. This study was carried out to detect changes in gene expression associated with both suicide and major depression using oligonucleotide microarrays (Affymetrix HG-U133 chip set) summarizing expression patterns in primarily ventral regions of the prefrontal cortex (BA44, 45, 46 and 47). A total of 37 male subjects were included in this study, of which 24 were suicides (depressed suicides = 16, nondepressed suicides = 8) and 13 were matched controls. All subjects were clinically characterized by means of psychological autopsies using structured interviews. Unique patterns of differential expression were validated in each of the cortical regions evaluated, with group-specific changes highlighting the involvement of several key neurobiological pathways that have been implicated in both suicide and depression. An overrepresentation of factors involved in cell cycle control and cell division (BA44), transcription (BA44 and 47) and myelination (BA46) was seen in gene ontology analysis of differentially expressed genes, which also highlights changes in the expression of genes involved in ATP biosynthesis and utilization across all areas. Gene misexpression in BA46 was most pronounced between the two suicide groups, with many significant genes involved in GABAergic neurotransmission. The pronounced misexpression of genes central to GABAergic signaling and astrocyte/ oligodendrocyte function provides further support for a central glial pathology in depression and suicidal behavior.

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Section: Discussionmentioning

confidence: 99%

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

et al. 2007

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“…Furthermore, although oxidative stress is suppressed in RAGE null and sRAGE-treated mice, it is not abolished. ADR also stimulates increases in S-100/ calgranulins, ligands linked to cell stress, [17][18][19][20] at least in part in podocytes.…”

Section: Discussionmentioning

confidence: 99%

RAGE Mediates Podocyte Injury in Adriamycin-induced Glomerulosclerosis

Jiang¹,

Ananthakrishnan²,

Qu³

et al. 2008

Journal of the American Society of Nephrology

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In the kidney, the receptor for advanced glycation end products (RAGE) is principally expressed in the podocyte at low levels, but is upregulated in both human and mouse glomerular diseases. Because podocyte injury is central to proteinuric states, such as the nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role of RAGE in podocyte damage. In this model, administration of the anthracycline antibiotic adriamycin provokes severe podocyte stress and glomerulosclerosis. In contrast to wild-type animals, adriamycin-treated RAGE-null mice were significantly protected from effacement of the podocyte foot processes, albuminuria, and glomerulosclerosis. Administration of adriamycin induced rapid generation of RAGE ligands, and treatment with soluble RAGE protected against podocyte injury and glomerulosclerosis. In vitro, incubation of RAGE-expressing murine podocytes with adriamycin stimulated AGE formation, and treatment with RAGE ligands rapidly activated nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, via p44/p42 MAP kinase signaling, and upregulated pro-fibrotic growth factors. These data suggest that RAGE may contribute to the pathogenesis of podocyte injury in sclerosing glomerulopathies such as focal segmental glomerulosclerosis.

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“…Tracing S100B may advance the extension of neuron axons and enhance the survival rate of neurons, while a great deal of it may generate toxic and side-effect [1]. A large number of activated S100B protein which is produced by glial cells is released into the extracellular after brain tissue injury [17], and then leaks into CSF and blood through damaged blood brain barrier, and S100B level in serum is positively correlated with the severity of the injury of cerebral ischemia [18]. Brouns and his group have also found that the concentration of S100B, which is in the cerebral spinal fluid (CSF) of the patients with acute ischemic stroke, is highly correlated to the severity of the injury and the prognosis of cerebral ischemia [19].…”

Section: Discussionmentioning

confidence: 99%

To Optimize the Therapeutic Dose and Time Window of Picroside II in Cerebral Ischemic Injury in Rats by Orthogonal Test

Huang¹,

Sun²,

Wang³

et al. 2013

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The paper aims to optimize the therapeutic dose and time window of picroside II by orthogonal test in cerebral ischemic injury in rats. The forebrain ischemia models were established by bilateral common carotid artery occlusion (BCCAO) methods. The successful models were randomly divided into sixteen groups according to orthogonal experimental design and treated by injecting picroside II intraperitonenally at different ischemic time with different dose. The concentrations of neuron-specific enolase (NSE), neuroglial marker protein S100B and myelin basic protein (MBP) in serum were determined by enzyme linked immunosorbent assay to evaluate the therapeutic effect of picroside II in cerebral ischemic injury. The results indicated that best therapeutic time window and dose of picroside II in cerebral ischemic injury were ischemia 1.5 h with 20 mg/kg body weight according to the concentrations of NSE, S100B and MBP in serum. It is concluded that according to the principle of lowest therapeutic dose with longest time window, the optimized therapeutic dose and time window are injecting picroside II intraperitonenally with 20 mg/kg body weight at ischemia 1.5 h in cerebral ischemic injury in rats.

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Active secretion of S100B from astrocytes during metabolic stress

Cited by 114 publications

References 15 publications

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

Altered expression of genes involved in ATP biosynthesis and GABAergic neurotransmission in the ventral prefrontal cortex of suicides with and without major depression

RAGE Mediates Podocyte Injury in Adriamycin-induced Glomerulosclerosis

To Optimize the Therapeutic Dose and Time Window of Picroside II in Cerebral Ischemic Injury in Rats by Orthogonal Test

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