Mentor: Dr. Stephanie Wohlgemuth
College of Agricultural and Life Sciences
"I became involved with research to intellectually challenge myself. Learning about new things is a passion of mine and being in the lab doing research allows me to constantly be thinking about how things work on a deeper level. Being involved with research has allowed me to see first hand how a project forms from planning to execution. I owe my mentor many thanks as she has supported me through every step of the process."
Animal Sciences- Animal Biology
- Autophagy Research
- Veterinary Research
- FL Academic Scholars Award (2011-2013)
- George Snow Scholarship Fund
- Your Community Foundation
- UF College of Veterinary Medicine Shelter Medicine Club
- Gainesville Pet Rescue
Hobbies and Interests
The Effects of Hydrogen Sulfide on Autophagy
Hydrogen sulfide (H2S) is an extremely toxic gas that, besides originating from inorganic sources, is produced by anaerobic bacteria that break down organic matter (Beauchamp et al., 1984). It can also be released by bacteria in both the mouth and gastrointestinal tract of mammals. In addition, it has recently been shown that small amounts of H2S are also produced endogenously by mammalian cells, and the gas is now considered the third gasotransmitter besides nitric oxide and carbon monoxide.
The main goal of this project is to determine by which mechanism H2S inhibits autophagy, how this inhibition affects cell viability, and whether it can be counteracted. This could be significant, given the cytoprotective effects of autophagy. Autophagy is one of the cellular housekeeping mechanisms by which intracellular components are degraded by lysosomes. More specifically, double-membrane vacuoles known as autophagosomes, containing intracellular constituents, fuse with lysosomes for breakdown of the engulfed cellular material.
To test the interaction of H2S with the autophagy-regulatory pathway, we will use cultured Saos-2 osteosarcoma cells. As a first step, I will confirm our preliminary results and expose cells that are either fed (in growth medium DMEM), starved (Krebs-Henseleit Buffer), or treated with rapamycin to different concentrations of H2S, using both hydrogen sulfide gas (as in our preliminary experiments) and H2S donors, such as Na2S salt. Subsequently, I will assess the autophagic response by quantifying the protein expression of the autophagy marker LC3, which localizes to the autophagosome, using gel electrophoresis and immunoblotting of cell lysates. As a second step, I will add specific inhibitors or activators of the autophagy-regulatory pathway to the above experimental design and determine their effect on the autophagic response in combination with H2S. In of doing this, we hope to target the specific point within the autophagic pathway in which hydrogen sulfide acts.