At Feinberg, I explored how an overlooked RNA-binding protein called SERBP1 might help regulate PAI-1, a molecule deeply involved in so many aging-related conditions including tissue fibrosis, obesity, and even Alzheimer’s disease. Prior research suggested that the location of SERBP1 within the cell (nucleus or cytoplasm) could control the stability of PAI-1 mRNA and ultimately how much of the PAI-1 protein is produced. I wanted to study if I could influence SERBP1’s location to control PAI-1 levels, which could open new possibilities for treating these conditions, especially cardiac fibrosis.
I designed experiments where I tagged SERBP1 with GFP to track its movement inside human cell models under different treatments, including high glucose conditions and small-molecule inhibitors. Alongside localization studies, I ran Western blots and qPCRs to quantify both PAI-1 and SERBP1 levels. Surprisingly, I found that high glucose conditions pushed SERBP1 into the cytoplasm, contradicting what existing literature suggested. But what was the most interesting was SERBP1’s potential prion-like (scaryyyy but it's not don't worry), transgenerational behavior, meaning its regulatory effects on PAI-1 could last across generations through epigenetic mechanisms. That long-lasting, real-world impact is something I have reinforced in my projects: holistically addressing these diseases.