Anita M's Senior Project Blog
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Project Title: Healing Heart Disease: What are the Effects of Overexpression of GRASP55 on ATF6 and GRP78? BASIS Advisor: John Goodwin Internship Location: University of Arizona School of Medicine, Phoenix Onsite Mentor: Dean Dr. Christopher Glembotski, Principal Investigator and Dr. Bethany Patton, Scientist III |
Project Abstract
Heart Disease is the leading cause of death in the United States. The American Heart Association estimates that every 40 seconds somebody experiences a heart attack, leading to around 800,000 Americans experiencing a heart attack every year. Around 300,000 of those heart attacks are fatal, but the remaining 500,000 people will experience eventual heart failure from cardiac hypertrophy as time goes by. So how can we stop this? Hypertrophy is a result of cell stress and when cells are stressed out for too long they die (which is what contributes to heart failure). ATF6 and GRP78 are genes that regulate cellular pathways to prevent cell stress. Similarly, GRASP55 is a protein that has also been found to play a vital role in preventing cell stress through a different mechanism. Because ATF6, GRP78, and GRASP55 individually help to combat cell stress and maintain homeostasis, we want to see if there is a relationship between the genes and the protein. This project can help us discover potential future targets to decrease cell stress, allowing us to delay or potentially prevent heart failure.
Week 11- I bid thee, farewell
Hey everyone! As we wrap up the last week, I've mostly been working on my final products. I've created a poster, a presentation, and a paper because I wanted to give multiple options for people to understand my project since everybody learns in different ways. This project was an incredible experience to get some first-hand... Read More
Week 10- Kick it!
Hey guys! The title of this blog is a little homage to track and field. On the final stretch of a race, you're supposed to "kick it," meaning use every ounce of energy you have left to cross the finish line. Needless to say, that's a little how this week has felt. I spent a... Read More
Week 9 – Writing the Days Away
Hey guys! In my previous post, I mentioned how we thought the tunicamycin (TM) treatment on my cells was either at too high of a dose or was left on the cells for too long, causing the cells to switch from survival mode (adaptive) to programmed cell death (maladaptive). And there is a way to... Read More
Week 8 – Plot Twist!
Hello everybody, This week we ran our qPCR to measure gene expression. After analyzing our data we noticed something off... Just as a quick reminder, previous literature has proved that ATF6 is activated in response to ER Stress. Tunicamycin (TM) causes ER Stress in Cells. Therefore, cells treated with TM should have increased expression of... Read More
Week 7- Taking and Making Genetic Material
Hello! In my last post, I mentioned treating my cells with tunicamycin (TM) to stress the cells, emulating the effects of a heart attack. The TM treatment worked well and we didn't experience a significant amount of cell death which was good! Below are pictures of my cells. The picture on the left is cells... Read More
Week 6- Third Time’s the Charm!
After making modifications to our protocol, we were able to add the GRASP55 plasmids to the cells with minimal cell death! We also plated only 400,000 cells this time, again, to avoid overcrowding in the wells. As you can see, compared to the last two trials of this experiment (in my last two posts), our... Read More
Week 5- Oops…I did it again
The original plan for this week was to repeat the experiment from last week. So we started to do that, but on the second step (transfecting the HEK cells with the GRASP55 plasmid), we experienced the same phenomenon as last time. Cells were peeling off the plate and dying in clumps. We originally hypothesized that... Read More
Week 4- What the HEK?!
This week I plated HEK293 cells into two six-well plates. Each well has roughly 750,000 cells suspended in 2 mL of media (media provides cells nutrients). Here's a picture of my cells! After plating, I incubated them overnight and added a GRASP55 plasmid and a control plasmid the next day. This plasmids are mixed with... Read More
Week 3- The Pathway that Bridges the Two: Introducing mTORC-1
The past few days consisted of signing my DCC form and completing online lab training. In the meantime, I am still reading through human physiology and pathology, as well as expanding my knowledge on GRASP55 (the protein of interest for my project). Here's a more detailed look at the link between GRASP55 and ATF6: When... Read More
Week 2- The Rough ER and Calcium’s Role in Heart Attacks
Much like the previous week, I have been studying human physiology and learning lots of cool fun stuff. For example, did you know that there is a high calcium concentration in the rough ER and a low calcium concentration in the cytosol. When Calcium ions move down that concentration gradient from the Rough ER and... Read More
Week 1- In Training…
The past week I have been working on acquiring more background information related to my project. This includes a lot of reading up on human physiology and pathology while continuing to edit my literature review. Attached is some pictures of my super legible notes discussing different types of lipids and proteins and their functions in... Read More
Introduction- Cardiovascular Disease
Hello! My name is Anita and my senior research project is on the effects of UPR Regulator ATF6 on the expression levels of ER Transmembrane Protein GRASP55 in cardiovascular disease. Your heart works from before your first breath to well after your last. This vital muscle works tirelessly to keep blood flowing throughout your body.... Read More