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J. Peter Gierow, Stina K. Carlsson, Daniel Diaz, Kaijin Wu, Sarah F. Hamm-Alvarez; Lymphocyte-Dependence of the Adenosine A2a Receptor Up-Regulation in the Male NOD Mouse Dry Eye Model. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3752.
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Studies in our laboratory have recently shown that adenosine potentiates the effect of carbachol on lacrimal gland secretion in rabbit through the A2 receptors (Curr. Eye Res. 2010, 35:466-474), and more recently that the adenosine A2a receptor is up-regulated in the male non-obese diabetic (NOD) mouse dry eye model (Invest. Ophthalmol. Vis. Sci. 51, E-abstract: p4139, 2010). In the present study, we have investigated the role of lymphocytes in the up-regulation of A2a receptors using NOD/SCID, a strain essentially lacking functional lymphocytes.
Lacrimal glands from 12 week old NOD, NOD/SCID, and BALB/c mice, the latter as a control, were used in this study. To detect adenosine receptor presence on mRNA level quantitative real-time PCR (qPCR) was performed. Immuno-histochemistry of sectioned cryonic lacrimal glands were used to detect protein expression.
The results revealed that the mRNA expression of the A2a receptor in lacrimal glands was higher in 12 weeks old NOD compared to BALB/c in the qPCR by 20-fold (p<0.001). A comparison between the strains showed that the A2a expression was 10-fold higher in NOD than in NOD/SCID (p<0.01), but no significant differences were obtained between NOD/SCID and BALB/c. Similar patterns were seen in the immuno-histochemistry, where A2a receptor staining was most intense in 12 weeks old NOD mice, and the increased staining was observed on both acinar cells and infiltrating lymphocytes.
Our results show that the up-regulation of the A2a receptor mRNA expression in the male NOD mice is at least partly lymphocyte-dependent, but that the immuno-staining is localized to both acinar cells and lymphocytes.
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