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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, RESULTS. Meshes: Apoptosis, Calcium Ionophores, Case-Control Studies, Cells, Cultured, Coronary Artery Disease, Coronary Vessels, Down-Regulation, Endothelial Cells, Human Umbilical Vein Endothelial Cells, Humans, Interleukin-11, Ionomycin, Leukocytes, Muscle, Smooth, Vascular, Myocytes, Smooth Muscle, Organ Culture Techniques, Recombinant Proteins, Signal Transduction, Tetradecanoylphorbol Acetate, Time Factors, Transforming Growth Factor beta1.
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Does activation of human vascular cells decrease their expression of transforming growth factor-beta? Context: Despite pro-fibrotic effects, transforming growth factor (TGF)-β prevents arteriosclerosis by suppressing effector leukocytes and promoting smooth muscle differentiation. However, previous observations of increased TGF-β expression in arteriosclerotic plaques are not consistent with that of an effective protective factor. We investigated the expression, regulation, and responses of TGF-β in human arterial tissues and cells. The expression of TGF-β by intrinsic vascular cells was lower in arteriosclerotic than non-diseased coronary arteries. Activation of resident and infiltrating leukocytes did not elicit TGF-β production from coronary artery segments in organ culture. Instead, the basal expression of TGF-β by coronary arteries decreased after vessel procurement and ex vivo culture. Activation of cultured smooth muscle cells and endothelial cells with phorbol ester and ionophore also decreased TGF-β expression. Isolated cell types representing those found in the artery wall were all capable of signaling in response to TGF-β, however production of the cytoprotective molecule, interleukin-11 was cell type-dependent and restricted to smooth muscle cells and fibroblasts. Interleukin-11 reduced smooth muscle cell apoptosis to T cell effectors.
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Inflammation and cellular activation diminish the basal expression of TGF-β by quiescent human vascular cells. Induction of interleukin-11 may contribute to the anti-arteriosclerotic actions of TGF-β. Final Decision: yes