Purchase this article with an account.
D.-A. M. Pillers, J. Pang, D. R. Trune; Enhanced Retinal Dystrophin Dp260 Upregulation by Glucocorticoid in MRL Autoimmune Mouse. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1715.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To determine whether upregulation of Dp260 expression occurs in vivo in response to exposure to a glucocorticoid drug.
Two normal mouse strains, C57BL/6J and Balb/c were chosen for study, and by serendipity, the autoimmune mouse strain MRL/MpJ-Fas(lpr) was also studied. These mice were receiving the glucocorticoid drug prednisolone as part of an unrelated study, and we were able to use the eyes in our work. Mice were treated with drug for 14-28 days then retinal gene expression for Dp260 was assayed by real-time quantitative RT-PCR using the ABI 7300 system. Assays were repeated in triplicate. The relative abundance of Dp260 mRNA was expressed as a ratio of treated to untreated baseline.
Dp260 expression was upregulated at the mRNA level in all three mouse strains when compared to baseline. Dp260 was upregulated 2-fold in the Balb/c mouse, and by nearly 6-fold in the C57BL/6J mouse. In the autoimmune MRL mouse, Dp260 expression was upregulated by 14-fold.
The observation that Dp260 can be upregulated in vitro by glucocorticoids is also of importance in the animal model. Dp260 upregulation may be one mechanism by which an enhanced b-wave response in the scotopic ERG has been shown in animals or individuals treated with glucocorticoid drugs. The MRL mouse is notable for its ability to regenerate tissue. It is defective in the Fas-proapoptosis pathway which may be important in either regeneration of, or preservation of photoreceptors during retinal disease. The substantial increase in expression of Dp260 in the autoimmune MRL mouse, as opposed to the control mice, suggests additional mechanisms by other genes that interact to modify the response to glucocorticoids in vivo.
This PDF is available to Subscribers Only