Intéraction P-sélection/PSGL-1 : impact sur l'agrégation et l'activation plaquettaire
Bibliographic record
Abstract
Platelet P-selectin binds to neufrophil P-$electin-Glycoprotein-Ligand-1 (PSGL-1) during inflammation and stabilizes platelet aggregation via a stili unknown mechanism.My projcet aims at evaluating the impact of P-selectinlPSGL-1 interaction on platelet biochemistry and function.In this study, P-selectin antagonism, using a blocking anti-P-selectin antibody or a recombinant PSGL-1 (rPSGL-Ig), slowed platelet aggregation under low thrombin (0.025 U/ml) stimulation and increased GPllbIffla antagonism (Reopro) potency.However, at a higher thrombin concentration (0.1 U/ml), aggregation was unaffected and Reopro' s potency diminished.Indeed, P-selectin-P$GL-l interaction was associated with increased platelet GPIIb/Illa activation, via a p38 mitogen-activated protein kinase (p38MAPK)-and cyclooxygenase (COX)-depcndent pathway.hi this connexion, tbromboxane A2 (TxA2) receptor blockade preserved the potency of Reopro and inhibited the increase in microaggregate formation afler P-selectinlPSGL-1 interaction.Also, the binding of neutrophil P$GL-1 to platelet P-selectin potentiated GPIIb/ffla activation and increased platelet maffix metalloprotease-2 (MMP-2) secretion and heteroaggregate formation.To further elucidate the mechanisms underlying P-selectin signaling, the role of the individual thrombin receptors, the protease-activated receptors 1 and 4 (PARi and PAR4), was studied.We found that following PARi stimulation, P-selectinlP$GL-i interaction only potentiates GPllbflfla activation, while afier PAR4 stimulation, in addition to GPllbfIlla activation, P-selectin transiocation and fibrinogen binding are also induced by P-selectinlPSGl-1 interaction.Moreover, increased platelet aggregation response and microaggregate formation are ffiggered by P-selectin signaling when platelet activation is regulated through PAR4, but flot PARi.In sum, interaction of platelet P-selectin wiffi PSGL-i induces platelet activation and influences platelet aggregation in response to thrombin via a TxA2-dependent increased microaggregate formation pathway and plateletineutrophil interaction via MMP-2 secretion.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.003 | 0.013 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.002 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.001 | 0.002 |
| Insufficient payload (model declined to judge) | 0.024 | 0.002 |
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 source (direct Gemma or distilled Codex), 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".