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Robert J. Walker, Jena J. Steinle; Role of β-Adrenergic Receptors in Inflammatory Marker Expression in Müller Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(11):5276-5281. doi: 10.1167/iovs.07-0129.
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purpose. To determine whether β-adrenergic receptors are involved in the modulation of inflammatory cytokines in Müller cells in a hyperglycemic environment.
methods. Rat Müller cells were grown in high (25 mM)- or low (5 mM)-glucose medium. Müller cells lysates were processed for real-time polymerase chain reaction to measure steady state mRNA expression for the following inflammatory markers: iNOS, TNF-α, IL-1B, and ICAM-1. Western blot analysis and ELISA assays were performed to determine the protein levels of these inflammatory markers and PGE2 content.
results. Isoproterenol treatment significantly decreased protein levels of iNOS, TNF-α, and IL-1B, in rMC-1 cells cultured in high glucose as early as 1 hour, compared with cells receiving no treatment. PGE2 content was also reduced after isoproterenol treatment. There were no significant changes observed in protein levels of ICAM-1 production after isoproterenol treatment in high glucose. Steady state mRNA levels for iNOS were significantly decreased 1 hour after isoproterenol, whereas ICAM-1 gene expression was significantly increased after 1 hour. Isoproterenol significantly increased gene expression for IL-1B after 24 hours of treatment.
conclusions. These results suggest that stimulation of β-adrenergic receptors with isoproterenol leads to decreased levels of PGE2, TNF-α, and IL-1B protein content, and in both gene expression and protein levels of iNOS in Müller cells cultured in hyperglycemia. β-Adrenergic receptor agonists had limited effects on ICAM-1 protein production. These results indicate that isoproterenol treatment reduces cytokine activation in cultured rat Müller cells.
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