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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Bevacizumab, Cell Survival, Coculture Techniques, Cytokines, Dexamethasone, Endothelium, Vascular, Fenofibrate, Humans, Interleukin-6, Retinal Vessels, Swine, Up-Regulation, Vascular Endothelial Growth Factor A, Vitreous Body.
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Is the in vitro response of human retinal endothelial cells to cytokines and other chemically active agents altered by coculture with vitreous-derived hyalocytes? Context: Ocular angiogenesis is regulated by polypeptides including cytokines, which are known to affect vascular endothelial cells. We have reported that hyalocytes interact with vascular endothelial cells, and some cytokines affect these interactions. To determine the effect of various chemically active agents on the viability of endothelial cells alone and cocultured with hyalocytes. The viability of human retinal endothelial cells (HRECs) was determined after exposure to IL-1alpha, IL-1beta, IL-6, TNFalpha and VEGF using the MTT assay. These results were compared to the viability when the HRECs were cocultured with porcine hyalocytes that had been exposed to different types of cytokines. The effects of bevacizumab, fenofibrate and dexamethasone on the viability of HRECs in coculture with hyalocytes were also assessed. Ten micrograms/millilitre of bevacizumab decreased the percentage of living HRECs stimulated by VEGF without hyalocytes, but with the hyalocytes, 100 microg/ml of bevacizumab was required to decrease the percentage of viable HRECs stimulated by VEGF. Fenofibrate, at 5 microg/ml, decreased the viability of HRECs stimulated by IL-1beta and VEGF without hyalocytes but could not decrease the viability of HRECs cocultured with hyalocytes. Dexamethasone, at 50 microg/ml, decreased the viability of HRECs stimulated by IL-1alpha, IL-1beta, IL-6 and VEGF without hyalocytes but could not decrease the viability of HRECs cocultured.
assistant
Coculturing HRECs with vitreous-derived hyalocytes depressed the effects of cytokines, bevacizumab, fenofibrate and dexamethasone. This suggests that the vitreal hyalocytes may play a role in pathogenic endothelial cell proliferation in vivo. Future studies to better understand this pathobiology should utilize coculture systems of HRECs and vitreal hyalocytes. Final Decision: yes