Abstract 3469: EphrinB2 promotes endothelial cell survival and vascular integrity
Bibliographic record
Abstract
Abstract EphrinB transmembrane ligands and their cognate EphB receptors critically contribute to vascular development through cell-to-cell signaling by the EphB receptor (forward signaling) and by the EphrinB ligand (reverse signaling). Previous studies demonstrated that mutant mice lacking ephrinB2 or EphB4 and a proportion of mice lacking EphB2 and EphB3 display severe defects in the embryonic vascular system and die at the embryo stage likely due to these vascular defects. Previously, we showed that EphB2, EphB4 and EphrinB2 are required for mature endothelial cell assembly into capillary structures. In the currently studies, we observed that silencing EphrinB2 expression in different types of primary human endothelial cells causes significant and time-dependent apoptotic cell death, as measured by cleavage of Poly(ADP-ribose) Polymerase (PARP), caspase-3 and caspase-8. VEGF, bFGF and SDF-1 variously modulated apoptosis induced by loss of EphrinB2 expression in endothelial cells. Gene expression profiling revealed that EphrinB2 silencing is associated with reduced expression of genes linked to regulation of the cell cycle progression and cytoskeleton organization, and with increased expression of pro-apoptotic genes. Breast cancer tissue from a patient treated with bevacizumab, a humanized monoclonal antibody that neutralizes VEGF, displayed evidence of endothelial cell apoptosis, which was associated with selectively reduced EphrinB2 expression, suggesting a link between VEGF signaling, EphrinB2 expression and cell death. These studies show that EphrinB2 expression is critical to endothelial cell survival in vitro and suggest that EphrinB2 contributes to blood vessel integrity in vivo. Thus, in addition to its well-characterized function as a regulator of cell-to-cell adhesion and repulsion, EphrinB2 is an endothelial pro-survival molecule, which may serve as a novel target for anti-angiogenic therapies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3469. doi:10.1158/1538-7445.AM2011-3469
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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 | 0.001 | 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 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.005 | 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".