Key result
Anti-TGF-beta1 antibody prevents L-NAME-induced cardiac inflammation and suppresses vascular inflammatory gene expression in rats.
We previously reported that chronic inhibition of nitric oxide (NO) synthesis with N(omega)-nitro-L-arginine methyl ester (L-NAME) induces inflammatory changes (monocyte infiltration, myofibroblast formation, and monocyte chemoattractant protein-1 [MCP-1] and transforming growth factor-beta1 [TGF-beta1] expression) in the rat heart and vessel. There is debate regarding whether TGF-beta1 exhibits proinflammatory or anti-inflammatory activities. We used the rat model to investigate the role of TGF-beta in the pathogenesis of such inflammatory changes. We show here that infiltrating monocytes and myofibroblasts in the inflammatory lesions produced TGF-beta1 on the third day of L-NAME administration. Cotreatment with a monoclonal antibody against TGF-beta1, but not with control IgG, prevented the L-NAME-induced cardiac inflammation. The antibody also significantly inhibited the gene expression of MCP-1, P-selectin, and intercellular adhesion molecule-1. In summary, the antibody against TGF-beta1 prevented inflammatory changes in rat heart and vessel induced by chronic inhibition of NO synthesis, suggesting that increased production of TGF-beta1 is involved in the inflammatory changes in this model.
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Koyanagi et al. (2000) studied Cardiovascular inflammatory changes induced by chronic inhibition of nitric oxide synthesis. Monoclonal antibody against TGF-beta1 vs. Control IgG was evaluated on Cardiac inflammation and inflammatory gene expression. Cotreatment with a monoclonal antibody against TGF-beta1 prevented L-NAME-induced cardiac inflammation and significantly inhibited MCP-1, P-selectin, and ICAM-1 gene expression in rats.
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