The Phenotype Changes of Astrocyte During Different Ischemia Conditions
Bibliographic record
Abstract
OBJECTIVES: Dementia is becoming a major health problem in the world, and chronic brain ischemia is an established important risk factor in predisposing this disease. Astrocytes, as one major part of the blood-brain barrier (BBB), are activated during chronic cerebral blood flow hypoperfusion. Reactive astrocytes have been classified into phenotype pro-inflammatory type A1 or neuroprotective type A2. However, the specific subtype change of astrocyte and the mechanisms of chronic brain ischemia are still unknown. METHODS: In order to depict the phenotype changes and their possible roles during this process, a rat bilateral common carotid artery occlusion model (BCAO) was employed in the present study. Meanwhile, the signaling pathways that possibly regulate these changes were investigated as well. RESULTS: After four-week occlusion, astrocytes in the cortex of BCAO rats were shown to be the A2 phenotype, identified by the significant up-regulation of S100a10 accompanied by the down-regulation of Connexin 43 (CX43) protein. Next, we established in vitro hypoxia models, which were set up by stimulating primary astrocyte cultures from rat cortex with cobalt chloride, low glucose, or/and fibrinogen. Consistent with in vivo data, the cultured astrocytes also transformed into the A2 phenotype with the up-regulation of S100a10 and the down-regulation of CX43. In order to explore the mechanism of CX43 protein changes, C6 astrocyte cells were handled in both hypoxia and low-glucose stimulus, in which decreased pERK and pJNK expression were found. CONCLUSIONS: In conclusion, our data suggest that in chronic cerebral ischemia conditions, the gradual ischemic insults could promote the transformation of astrocytes into A2 type instead of A1 type, and the phosphorylation of CX43 was negatively regulated by the phosphorylation of ERK and JNK. Also, our data could provide some new evidence of how to leverage the endogenous astrocytes phenotype changes during CNS injury by promoting them to be "protector" and not "culprit".
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".