S100B secretion is stimulated by IL-1β in glial cultures and hippocampal slices of rats: Likely involvement of MAPK pathway

Souza, Daniela Fraga de; Leite, Marina Concli; Quincozes‐Santos, André; Nardin, Patrícia; Tortorelli, Lucas Silva; Rigo, Maurício; Gottfried, Carmem; Leal, Rodrigo Bainy; Gonçalves, Carlos-Alberto

doi:10.1016/j.jneuroim.2008.10.012

Cited by 58 publications

(36 citation statements)

References 44 publications

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“…Furthermore, the extracellular release of S100B can be triggered by a number of stimuli, including TNF-␣, IL-1␤, and A␤ [48][49][50]. While many studies have strongly implicated a role for S100B in AD (e.g., see [26,51]), the results here suggest that elevated S100B levels may be related to increased severity in specific populations.…”

Section: Discussionmentioning

confidence: 50%

Neurodegenerative Markers are Increased in Postmortem BA21 Tissue from African Americans with Alzheimer’s Disease

Ferguson

Panos

Sloper

et al. 2017

JAD

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Abstract.Background: Alzheimer's disease (AD) presents with an earlier onset age and increased symptom severity in African Americans and Hispanics. Objective: Although the prevalence of plaques and tangles may not exhibit ethnicity-related differences, levels of neurodegenerative proteins have not been described. Methods: Here, levels of five proteins (i.e., S100B, sRAGE, GDNF, A␤ 40 , and A␤ 42 ) and the A␤ 42 /A␤ 40 ratio were measured in postmortem samples of the middle temporal gyrus (BA21) from age-matched African Americans and Caucasians with AD (n = 6/gender/ethnicity). Results: S100B levels were increased 17% in African Americans (p < 0.003) while sRAGE was mildly decreased (p < 0.09). A␤ 42 levels were increased 121% in African Americans (p < 0.02), leading to a 493% increase in the A␤ 42 /A␤ 40 ratio (p < 0.002). Analysis of GDNF levels did not indicate any significant effects. There were no significant effects of gender and no significant ethnicity with gender interactions on any analyte. Effect size calculations indicated "medium" to "very large" effects. Conclusion: S100B is typically elevated in AD cases; however, the increased levels in African Americans here may be indicative of increased severity in specific populations. Increased A␤ 42 /A␤ 40 ratios in the current study are compatible with increased disease severity and might indicate increased AD pathogenesis in African Americans. Overall, these results are compatible with a hypothesis of increased neuroinflammation in African Americans with AD.

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Section: Discussionmentioning

confidence: 50%

Neurodegenerative Markers are Increased in Postmortem BA21 Tissue from African Americans with Alzheimer’s Disease

Ferguson

Panos

Sloper

et al. 2017

JAD

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“…Primary rat cortical astrocytes were stimulated with low levels of IL-1β to mimic a reactive phenotype (5,6). After 24 h, conditioned media from stimulated astrocytes showed a clear accumulation of soluble HMGB1 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Astrocytic high-mobility group box 1 promotes endothelial progenitor cell-mediated neurovascular remodeling during stroke recovery

Hayakawa

Pham

Katušić

et al. 2012

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

160

154

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Crosstalk between the brain and systemic responses in blood is increasingly suspected of playing critical roles in stroke. However, how this communication takes place remains to be fully understood. Here, we show that reactive astrocytes can release a damage-associated molecular-pattern molecule called high-mobilitygroup-box-1 (HMGB1) that promotes endothelial progenitor cell (EPC)-mediated neurovascular remodeling during stroke recovery. Conditioned media from reactive astrocytes increase EPC proliferation in vitro. siRNA suppression of HMGB1 in astrocytes or blockade of the HMGB1 receptor for advanced glycation endproducts in EPCs prevents this effect. In a mouse model of focal cerebral ischemia, reactive astrocytes in the peri-infarct cortex upregulate HMGB1 at 14 d poststroke, along with an accumulation of endogenous EPCs. In vivo siRNA suppression of HMGB1 blocks this EPC response, reduces peri-infact angiogenesis, and worsens neurological deficits. Taken together, these molecular and in vivo findings support a previously undescribed mechanism of crosstalk between reactive astrocytes and EPCs wherein HMGB1 promotes neurovascular remodeling and functional recovery after stroke and brain injury.reactive glia | vascular repair | brain remodeling

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“…Late passage cells (i.e., after at least 100 passages) were seeded in 24-well plates at densities of 10 4 cells/well, then cultured in DMEM (pH 7.4) supplemented with 5% fetal bovine serum, 2.5 mg/ mL amphotericin B, and 100 U/L gentamicin in 5% CO 2 / 95% air at 378C (de Souza et al, 2009). After cells reached confluence, the culture medium was replaced by DMEM without serum in the absence or presence of GJ blockers or GZA.…”

Section: C6 Glioma Cell Culturementioning

confidence: 99%

Gap junction inhibitors modulate S100B secretion in astrocyte cultures and acute hippocampal slices

Leite

Galland

Souza

et al. 2009

J of Neuroscience Research

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Astrocytes sense, integrate, and respond to stimuli generated by neurons or neural injury; this response involves gap junction (GJ) communication. Neuronal vulnerability to injury increased when cocultures of astrocytes and neurons were exposed to GJ inhibitors. However, GJ uncoupling could limit the extension of a lesion. We investigated a possible link between GJ communication and S100B secretion. S100B is a calcium-binding protein of 21 kDa that is predominantly expressed and secreted by astrocytes, which has trophic paracrine activity on neurite growth, glial proliferation, and neuronal survival. GJ inhibitors were analyzed in isolated astrocytes in primary cultures from hippocampus, acute hippocampal slices, and C6 glioma cells, which were used as a negative control. Our data indicate that GJ blocking stimulates S100B secretion in astrocyte cultures and acute hippocampal slices. Different assays were used to confirm cell integrity during exposure to GJ inhibitors. S100B secretion was observed with different types of GJ inhibitors; the resulting event was dependent on time, the nature of the inhibitor, its putative molecular target of GJ blocking, and/or the cell preparation used. Only carbenoxolone induced a fast and persistent increase in S100B secretion in both preparations. Endothelin-1 increased S100B secretion in astrocyte cultures at 1 hr, but a decrease was observed at 6 hr or in acute hippocampal slices. Physiologically, a local GJ closure associated with release of S100B in injury conditions favors the idea of a common mechanism available to limit the extension of lesion and increase the chances of cell survival.

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S100B secretion is stimulated by IL-1β in glial cultures and hippocampal slices of rats: Likely involvement of MAPK pathway

Cited by 58 publications

References 44 publications

Neurodegenerative Markers are Increased in Postmortem BA21 Tissue from African Americans with Alzheimer’s Disease

Neurodegenerative Markers are Increased in Postmortem BA21 Tissue from African Americans with Alzheimer’s Disease

Astrocytic high-mobility group box 1 promotes endothelial progenitor cell-mediated neurovascular remodeling during stroke recovery

Gap junction inhibitors modulate S100B secretion in astrocyte cultures and acute hippocampal slices

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