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Faculty Mentor

Judith D. Ochrietor, PhD

Faculty Mentor Department

Department of Biology

Abstract

Chronic inflammation is a current public health concern as it is linked to the etiology and symptoms of numerous diseases, for example diabetic retinopathy (DR). In the case of DR, inflammation leads to dysregulation of the blood retina barrier causing retinal hemorrhage and macular edema leading ultimately to irreversible vision loss. MCT-1 is critical for the survival of photoreceptor cells because MCT-1 forms protein complexes with Basigin, a cell-cell adhesion protein, that enables Müller glial cells to efficiently provide lactate as a high energy fuel source. Previous studies have shown chronic inflammation reduces Basigin expression in the retina and that MCT-1 relies on Basigin to attain proper position in the cell membrane. Thus, the aim of the present study was to investigate MCT-1 expression in response to chronic inflammation within the retina. Mouse retinas harvested at post-natal days 7 and 30 were incubated in culturing medium containing lipopolysaccharide (LPS, 100 μg/mL), a known inflammatory agent, or the same volume of phosphate buffered saline (PBS) for 24 hours to mimic chronic inflammation. Concentrations of MCT-1 were then quantified by ELISA. No significant difference in MCT-1 protein expression was observed between the LPS- and PBS-treated samples at either age. This suggests that chronic inflammation does not affect MCT-1 protein expression within the retinal environment at neonatal and adolescent age groups, however, future investigations with older mice may produce different results.

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