ENDOTHELIAL GAS6 Contributes to Thrombogenesis and Promotes TISSUE FACTOR Upregulation DURING Vessel Injury
Bibliographic record
Abstract
Abstract Abstract 702 Gas6 is a vitamin K-dependent, secreted protein that amplifies platelet aggregation and secretion in response to platelet agonists. Gas6−/− mice are protected from experimentally induced lethal venous and arterial thromboembolism. This protection has been attributed to defective aggregation in platelets from gas6−/− mice. However, this platelet phenotype was only observed when platelets were challenged by only one agonist, ADP, and only at a concentrations of 5.0μM. This subtle platelet abnormality resulting in a rather dramatic clinical phenotype raise the possibility that gas6 from a source other than platelets contributes to thrombus formation. We hypothesize that gas6 derived from the endothelium plays a role in venous thrombus formation. Gas6−/− mice are protected against venous thrombosis induced by 0.37 M FeCl3 in the inferior vena cava (IVC). Bone marrow transplantation experiments generating mice with selective ablations of gas6 from either the hematopoietic or non-hematopoietic compartments demonstrate an approximately equal contribution by gas6 from both compartments to thrombus formation. Platelet depletion in wild type or gas6−/− mice followed by reconstitution with platelets from either WT or gas6−/− mice confirm that gas6 from compartments other than the platelet contribute to thrombosis development. Furthermore, gas6−/− mice are hyporesponsive to FeCl3 mediated tissue factor induction in venous endothelium, as observed by immunofluorescence staining and later validated by a functional assay. In addition, in vitro, gas6−/− endothelial cells are hyporesponsive to thrombin mediated tissue factor mRNA induction. Taken together, these results suggest that non-hematopoietic gas6, possibly from the endothelium, contributes to thrombus formation in vivo and can be explained by the ability of gas6 to promote endothelial tissue factor induction. These findings support the notion that endothelial gas6 may play a pathophysiologic role in venous thromboembolism. Disclosures: No relevant conflicts of interest to declare.
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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 | 0.000 | 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 | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.001 |
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".