Activation of CD36 Inhibits and Induces Regression of Inflammatory Corneal Neovascularization
Bibliographic record
Abstract
PURPOSE: This study was undertaken to investigate the role of the antiangiogenic receptor CD36 during inflammatory corneal neovascularization (CNV). METHODS: In a murine model of inflammatory CNV, CD36 expression was evaluated by RT-PCR and immunofluorescence. Mice subjected to CNV were treated topically (thrice daily) with CD36 functionally neutralizing antibodies against the oxidized low-density lipoprotein (oxLDL) and thrombospondin (TSP)-1 sites (clones JC63.1 and FA6-152, respectively). Neovascularization was analyzed by CD31-immunostained corneal flatmounts. The role of the less characterized oxLDL site during angiogenesis was elucidated by using the CD36 ligand 1-palmitoyl 2-(5'-oxovaleroyl) phosphatidylcholine (POVPC; 50, 100 microg/mL) 24 hours after corneal injury for 7 days, whereas in angioregressive studies, POVPC treatments were initiated 10 days after induction of CNV. In this process, VEGF expression was also studied. Effects of CD36 activation were further examined ex vivo using the mouse aortic ring assay. RESULTS: CD36 expression was upregulated after corneal injury; CD36 was expressed in corneal epithelium, limbus, invading microvessels, and stromal macrophages. Blocking CD36 activity with FA6-152 significantly increased CNV (P <0.001). Conversely, activating CD36 with POVPC dose dependently inhibited CNV (P = 0.003); this effect was blocked by JC61.3. POVPC also significantly regressed preformed blood vessels (P < 0.001). Ex vivo experiments on aortic rings confirmed the angioinhibitory and -regressive effects of POVPC. Because corneal macrophages express CD36 and may partake in angiogenesis via VEGF-A secretion, we surmised that VEGF-A could be modulated by CD36. Indeed, POVPC downregulated VEGF-A expression in a time-dependent fashion (P < 0.001), whereas FA6-152 induced its expression (P < 0.05). CONCLUSIONS: CD36 is involved both physiologically and pharmacologically in inhibition and regression of CNV, by direct effect on endothelial cells and partly by negatively regulating VEGF expression in macrophages.
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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 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 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 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".