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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: Blood Flow Velocity, Cells, Cultured, E-Selectin, Endothelium, Vascular, Enzyme-Linked Immunosorbent Assay, Humans, Immunoblotting, Interleukin-1, Oncostatin M, Peptides, Phorbol Esters, Protein Biosynthesis, Proteins, RNA, Messenger, Transcription, Genetic, Tumor Necrosis Factor-alpha, Umbilical Veins.
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Does fluid flow regulate E-selectin protein levels in human endothelial cells by inhibiting translation? Context: The purpose of this study was to determine the mechanism with which fluid flow inhibits endothelial E-selectin expression. Cultured human umbilical vein endothelial cells were stimulated with inflammatory agonists (tumor necrosis factor-alpha [TNF-alpha], interleukin-1beta, oncostatin M, or phorbol ester) in the presence or absence of fluid flow (peak shear stress, approximately 12 dynes/cm(2)) imposed with an orbital shaker. E-selectin expression was assessed with ribonuclease protection assay, immunoblotting, enzyme-linked immunosorbent assay, or metabolic labeling as appropriate. All agonists caused human umbilical vein endothelial cells to express E-selectin protein. Fluid flow inhibited E-selectin protein levels by about 50% in response to TNF-alpha but had no effect on total E-selectin messenger RNA (mRNA) expression. Flow inhibited E-selectin protein production even after initiation of E-selectin transcription. Flow did not cause E-selectin to be shed from the cell surface nor was E-selectin degradation accelerated. Although fluid flow did not reduce total cellular E-selectin mRNA levels in response to TNF-alpha, the amount of E-selectin mRNA present in the actively translated polysome fraction was markedly attenuated.
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These findings indicate that E-selectin expression is subject to translational and transcriptional control. Fluid mechanical forces can regulate endothelial phenotype by targeting translational control points. Final Decision: yes