Starting in the spring of my freshman year, I became involved in my research projects at the Dichek lab. When I first arrived at the lab I unable to pipette correctly. Yet, with the help of the Post Doctoral researcher I work with, I was soon participating in gene therapy research to help treat atherosclerosis. Throughout my time in the Dichek lab, I learned basic microbiology and biochemistry lab techniques, applied what I have learned in statistics courses, and helped plan for a new and upcoming experiment.
In addition to learning these valuable laboratory techniques, I learned how to refine my curiosity into actionable items. When I first started working in the Dichek lab, I was very excited and overeager to contribute my ideas to the team. Through talks with my in-lab mentors, I learned how to critically analyze literature for new ideas and directions, ask testable questions and carry out experiments. In this process, I learned that techniques and raw enthusiasm does not make a researcher, it is persistence and well-thought out designs.
Over the few years I have worked in the Dichek lab, I have slowly gained more autonomy and independence in the projects that I help run or assist. On a whole, I have spent most of my time with the gene therapy arm of the lab. This entailed artificially increasing the expression of atheroprotective genes, such as ABCA1 and ApoAI.
The project that I worked on focused on the over-expression of ABCA1. This involved transfecting endothelial cells with a modified virus loaded with the ABCA1 gene. While this therapy was shown to be highly effective, there were associated limitations. Specifically, the viral vector could not travel though the layer of endothelial cells to the atherosclerotic plaque. This led my mentor and I to utilize exosome-loading of microRNA. This project utilized an indirect route of ABCA1 over-expression. As part of the native genome, the micro-RNA miR-33a-5p inhibits the expression of ABCA1. We utilized a specific sequence of nucleotides to tag a therapeutic micro-RNA that inhibits miR-33a-5p. This allowed it to be loaded into exosomes and delivered to other cells. As a result we found that miR-33a-5p expression fell, which coincided with a rise in ABCA1 expression. This rise in ABCA1 expression has the potential to almost completely remove plaque that causes cardiac related pathologies.
Overall, my research experience at UW has focused on potential change in the way we treat cardiovascular disease. I believe that the projects that I have worked on could have an enormous impact within my own lifetime by improving patient outcomes and pioneering new ways to regulate aberrant gene expression. While not exactly what I thought I would have spent the majority of my time at UW doing, research has become an integral part of my life. As such, I hope that I have the opportunity to continue doing meaningful research in my future.
In addition to learning these valuable laboratory techniques, I learned how to refine my curiosity into actionable items. When I first started working in the Dichek lab, I was very excited and overeager to contribute my ideas to the team. Through talks with my in-lab mentors, I learned how to critically analyze literature for new ideas and directions, ask testable questions and carry out experiments. In this process, I learned that techniques and raw enthusiasm does not make a researcher, it is persistence and well-thought out designs.
Over the few years I have worked in the Dichek lab, I have slowly gained more autonomy and independence in the projects that I help run or assist. On a whole, I have spent most of my time with the gene therapy arm of the lab. This entailed artificially increasing the expression of atheroprotective genes, such as ABCA1 and ApoAI.
The project that I worked on focused on the over-expression of ABCA1. This involved transfecting endothelial cells with a modified virus loaded with the ABCA1 gene. While this therapy was shown to be highly effective, there were associated limitations. Specifically, the viral vector could not travel though the layer of endothelial cells to the atherosclerotic plaque. This led my mentor and I to utilize exosome-loading of microRNA. This project utilized an indirect route of ABCA1 over-expression. As part of the native genome, the micro-RNA miR-33a-5p inhibits the expression of ABCA1. We utilized a specific sequence of nucleotides to tag a therapeutic micro-RNA that inhibits miR-33a-5p. This allowed it to be loaded into exosomes and delivered to other cells. As a result we found that miR-33a-5p expression fell, which coincided with a rise in ABCA1 expression. This rise in ABCA1 expression has the potential to almost completely remove plaque that causes cardiac related pathologies.
Overall, my research experience at UW has focused on potential change in the way we treat cardiovascular disease. I believe that the projects that I have worked on could have an enormous impact within my own lifetime by improving patient outcomes and pioneering new ways to regulate aberrant gene expression. While not exactly what I thought I would have spent the majority of my time at UW doing, research has become an integral part of my life. As such, I hope that I have the opportunity to continue doing meaningful research in my future.