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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, METHODS, RESULTS. Meshes: Animals, Caveolin 1, Cell Line, Cytokines, Gene Expression, Genetic Vectors, Humans, Inflammation, Lentivirus, Lipopolysaccharides, Male, Mice, Mice, Inbred C57BL, NF-kappa B, Phospholipases A2, Cytosolic, Pulmonary Alveoli, p38 Mitogen-Activated Protein Kinases.
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Do over-expression of caveolin-1 aggravate LPS-induced inflammatory response in AT-1 cells via up-regulation of cPLA2/p38 MAPK? Context: The aim of this study was to study the effect of caveolin-1 on the cytosolic phospholipase A2 (cPLA2), p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappaB (NF-kappaB) in mouse lung alveolar type-1 cells' (AT-1 cells) inflammatory response induced by LPS. Gene clone technique was used to over-express caveolin-1 in AT-1 cells by lentivirus vector. The level of tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), cPLA2, p38 MAPK and NF-kappaB was measured by ELISA, western blotting and EMSA. AT-1 cells were treated with LPS. Over-expression of caveolin-1 not only increased the production of pro-inflammatory cytokine TNF-alpha and IL-6, but also enhanced the expression of the cPLA2, p38 MAPK, and NF-kappaB.
assistant
Our data demonstrated that over-expression of caveolin-1 aggravates the AT-1 injury induced by LPS, involving in modulation of the cPLA2 mediated by the cPLA2/p38 MAPK pathway. Final Decision: yes