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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: OBJECTIVE, METHODS, RESULTS. Meshes: Analysis of Variance, Apoptosis, Cells, Cultured, Drug Interactions, Enzyme-Linked Immunosorbent Assay, Epidermal Growth Factor, Epithelial Cells, Flow Cytometry, Heparin-binding EGF-like Growth Factor, Humans, Intercellular Signaling Peptides and Proteins, Interferon-gamma, Interleukin-1, Intestinal Mucosa, Probability, Reference Values, Sensitivity and Specificity, Tumor Necrosis Factor-alpha.
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Does heparin-binding EGF-like growth factor decrease apoptosis in intestinal epithelial cells in vitro? Context: The production of heparin-binding EGF-like growth factor (HB-EGF) is upregulated during organ injury and has a cytoprotective effect during hypoxic stress in intestinal epithelial cells in vitro and intestinal ischemia-reperfusion injuries in vivo. The purpose of this study was to determine if HB-EGF-related cytoprotection is manifested through alterations in apoptosis. Human intestinal epithelial cell monolayers (DLD-1 and Caco-2) were stimulated with interleukin (IL)-1 (20 ng/mL), tumor necrosis factor (TNF)-alpha (40 ng/mL), and interferon (IFN)-gamma (10 ng/mL) with or without HB-EGF (1, 10 or 100 ng/mL) and analyzed for rates of apoptosis utilizing a Cell Death Detection ELISA and flow cytometry. ELISA results showed a 3-fold increase in the level of apoptosis during stimulation with cytokines compared with nonstimulated cells (P <.05). Relative levels of cytokine induced apoptosis were reduced after 12 hours of HB-EGF exposure (P <.05) in a dose-dependent fashion. Results of flow cytometric analysis also showed a reduction in apoptosis at 6 hours when cell monolayers were stimulated with cytokines in conjunction with HB-EGF compared with cytokines alone (P <.05).
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HB-EGF downregulated apoptosis in intestinal epithelial cells exposed to proinflammatory cytokines in vitro. The results of this study suggest that alterations in apoptosis may represent a possible mechanism by which this growth factor exerts its cytoprotective effect at the mucosal level during the proinflammatory state. Final Decision: yes