The Effect Of Progranulin On Lysosomal Function In Bv2 Cells
Abstract
Neurodegenerative diseases afflict nearly 7 million people in United states, constituting a significant portion of the 600 known neurological disorders. Characterized by the gradual loss of neurons and axons within the central nervous system (CNS), these conditions stem from chronic inflammatory activation of the brain. Chronic inflammation disrupts important processes such as autophagy lysosome pathway, a self-degradative process that eliminates protein aggregates and damaged organelles. Trehalose, a non-reducing disaccharide that triggers autophagic flux in neuronal cells and promotes the clearance of protein aggregates; however, without understanding the mechanism behind how trehalose affects these functions, it lacks value. In our study, we aim to identify the role of trehalose in autophagy under inflammation. The explicit mechanism of how trehalose provides neuroprotection remains unknown; however, taken together, our hypothesis posits that trehalose improves lysosomal function in BV2 cells under oxidative stress and neuroinflammation. Our research shows that trehalose restores the levels of autophagy markers after the induction of oxidative stress and inflammation in BV2 cells. The level of LAMP 1, LC3, p62 soluble and insoluble fractions were restored when treated with trehalose. With the completion of our study, we anticipate that our findings will provide sufficient evidence that trehalose is important to maintain neuroprotection in inflammatory state by upregulating autophagy, potentially providing trehalose based therapeutics. KEYWORDS: trehalose, neuroinflammation, lysosomal function, autophagy, inflammation, microglial cells
