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Assessing Mitochondrial Quality Control in Primary Trabecular Meshwork
Location: 51
Mentor: Dr. Anh Pham
Mitochondrial dysfunction plays a role in many diseases, including glaucoma. Impaired trabecular meshwork (TM) cell function contributes to elevated intraocular pressure (IOP) in glaucoma, primarily due to increased aqueous humor resistance from TM stiffness. Mitophagy, the selective degradation of mitochondria, and biogenesis are essential for mitochondrial health and cellular homeostasis. UA, a metabolite that enhances mitophagy, will be examined for its effects on mitochondrial dysfunction in TM cells. Understanding mitochondrial regulation mechanisms may open therapeutic methods for improving TM health and mitigating age-related mitochondrial decline in glaucoma. Protein concentrations were quantified using the BSA protein assay. Western blot analysis was performed on 20 µg of each sample separated on SDS-PAGE gels (8%, 10%, 12%) and transferred to PVDF membranes. Membranes were blocked with 5% non-fat milk in TBST, followed by incubation with primary antibodies (1:1000) at 4°C overnight. HRP-conjugated secondary antibodies (1:10000) were incubated for 1 hour at room temperature. Protein bands were detected via chemiluminescence, imaged, and quantified using Gel analyzer software and normalized to GAPDH levels. Primary TM cells were cultured and confirmed by Dex-induced myocilin expression. Mitophagy induction by UA (50 µM) was analyzed via Western blot, identifying key proteins involved. Significant increases (p
