(482.40) Finasteride induces Epigenetic Modulation of LSP1: A Gene implicated in Neutrophil Actin Dysfunction disease

Poster Board Number: C155
Introduction: AAA has separate poster presentation times for odd and even posters.
Odd poster #s – 10:15 am – 11:15 am
Even poster #s – 11:15 am – 12:15 pm

Churchill Ihentuge (University of Pikeville), Anthonei Csoka (Howard University)

Lymphocyte Specific Protein 1 (LSP1) gene translates F-actin protein expressed in leucocytes such as neutrophils, lymphocytes, macrophages, and endothelium. It controls neutrophil motility, adhesion to fibrinogen matrix proteins, and transendothelial migration. Overexpression or increased level of Lymphocyte Specific Protein 1 (LSP1) is implicated in a rare immunologic disorder Neutrophil Actin Dysfunction characterized by spontaneous onset of recurrent infections and inflammation of oral cavity, skin, and respiratory tract. In this experiment aimed at studying the methylation profile and genes expression following finasteride treatment, we cultured human Leydig cells in the presence of 0.5 μM finasteride for 14 days and performed whole-genome DNA methylation analysis using the NimbleGen Human DNA Methylation 3×720K Promoter Plus CpG Island Array and Ingenuity Pathway Analysis. Results identified several genes that were differentially methylated following finasteride treatment. Lymphocyte Specific Protein 1 (LSP1) gene was downregulated through methylation. We therefore deduced that finasteride could be a gateway to the treatment of Neutrophil Actin Dysfunction disease through epigenetic modification and decreased expression of LSP1 gene.