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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, METHODS, RESULTS. Meshes: Actin Cytoskeleton, Arginine, Cell Nucleus, Cytochalasin D, DNA, Depsipeptides, Human Umbilical Vein Endothelial Cells, Humans, Intercellular Adhesion Molecule-1, NF-kappa B, Protein Binding, Protein Transport, Stress Fibers, Transcription Factor RelA.
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Does actin cytoskeleton modulate ADMA-induced NF-kappaB nuclear translocation and ICAM-1 expression in endothelial cells? Context: Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor, increases the activity of NF-κB (NF-κB) and then induces the expression of intercellular adhesion molecule-1 (ICAM-1). However, the mechanisms regulating ADMA-induced NF-κB activation are unknown. This study investigated the function of actin cytoskeleton for ADMA-induced NF-κB activation and ICAM-1 expression in endothelial cells. Human umbilical vein endothelial cells (HUVEC) were cultured and left untreated or challenged for 24 h with 100 µM ADMA in the absence and presence of 5 µM cytochalasin D (Cyt D), or 1 µM Jasplakinolide (Jas). The form of actin cytoskeleton, the translocation of NF-κB, NF-κB DNA binding activity, and the expression of ICAM-1 were determined. ADMA increased the formation of stress fiber in endothelial cells, and Cyt D clearly induced destabilization of the actin filaments. Either stabilizing or destabilizing the actin cytoskeleton prevented ADMA-induced NF-κB activation. It also showed that the inhibition of NF-κB activity was due to the impaired NF-κB nuclear translocation. Further, stabilizing or destabilizing the actin cytoskeleton inhibited the expression of the NF-κB target protein, ICAM-1.
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Actin cytoskeleton may be engaged in modulated ADMA-induced NF-κB activation and thereby ICAM-1 expression in endothelial cells. Final Decision: yes