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Description

Oxidative damage is caused by an imbalance in the production and accumulation of the reactive oxygen species (ROS) due to oxidative stress. The Bhattacharjee lab is studying the relationship between oxidative damage and lipoprotein receptor-related protein (LRP- 1) signaling. LRP-1 signaling is important because it may be involved in cell migration and invasion. This, in turn, may control RPE cell movement and invasion through the expression of LRP-1. We used diabetic mice that were homozygous for the spontaneous mutation Leprdb along with the non-diabetic heterozygous controls and treated them with 100μM apoEdp. Treatment started at 12 weeks of age for all mice and the mice were sacrificed at 24 weeks. Western blot and immunohistochemical analyses were done to study neural apoptosis and LRP-1 targeted signaling pathways. It was found that treatment of LRP-1 targeted apoEdp resulted in the inactivation of cytoplasmic protein phosphatases PP2A, increase in intracellular kinase activity of PI3K/Akt and ERK1/2 pathways, significant reduction in retinal ganglionic cell death, and inhibition of proapoptotic BCL-2 associated death (BAD) and cleaved caspase 3. We plan to study the LRP-1 signaling and BRB integrity in obesity-induced type 2 diabetic mice. Using the combined data of the diabetic and induced diabetic mice, our overall goal is to utilize this data and apply this to how oxidative stress treatment of human retinal pigment epithelium (hRPE) affects endocytosis through LRP-1 and intracellular phosphatase/kinase signaling.

Publication Date

2021

City

New Orleans

Keywords

Microbiology, Oxidative Damage, Signaling, Retinal Pigment, Epithelial Cells

Disciplines

Biology | Life Sciences | Microbiology

Oxidative Damage and LRP-1 Signaling in Retinal Pigment Epithelial Cells

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