Romay, Milagros (2012 - 2016)
Millie is in the Department of Microbiology, Immunology and Molecular Genetics. She joined the training program in 2012. Her research mentor is Dr. Jake Lusis. She received a B.S. degree in 2010 from UCLA.
Mentor: Dr. Jake Lusis
Atherosclerotic lesion formation is hypothesized to be initiated by the accumulation of low density lipoprotein (LDL) in the vessel wall. LDL is then modified through exposure to reactive oxygen species to form minimally modified LDL (mmLDL).Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphatidylcholine (OX-PAPC) is the major phospholipid in mmLDL that induces inflammation in human aortic endothelial cells (HAECs). Treatment of cultured HAECs with OX-PAPC is known to change the expression of hundreds of genes in comparison to untreated cells. However the mechanism of OX-PAPC regulation for many of these genes is unknown. We hypothesized that microRNAs (miRNAs) played a role in this regulation therefore we used next generation sequencing to identify miRNAs that were regulated by OX-PAPC. We identified two miRNAs that were upregulated by OX-PAPC treatment. Analysis of whole genome transcript profiling in cells overexpressing these two miRNAs predicted that the miRNAs were involved with the regulation of NF- κB signaling. Ongoing experiments are focused on identifying the key miRNA target genes responsible for the effects on NF-κB signaling.
