Madeline working in the Gladstone Institutes' Stem Cell Core.
Madeline working in the Gladstone Institutes' Stem Cell Core.
“Before I started at CCSF, I had just earned a B.A. in Psychology and had been working as an assistant dog groomer while figuring out my next steps. I had always been interested in biology and medicine but had been discouraged by some challenges I experienced while in college. I wanted to try out a career in biotech, without accumulating even more student debt.
The biotech program at CCSF allowed me to gain both a background in biology and experience in the lab, while also working part-time. I was able to determine if biotech was a good fit for me without a huge investment of time and money. I enjoyed the program so much that I went on to complete the CIRM-funded stem cell internship this past year.
After my internship, I will join the Conklin Lab at Gladstone Institutes as a research associate. My experience working with stem cells and CRISPR technology got me a job in a well-known biomedical research lab, all thanks to the biotech program at CCSF. I plan to further my education with a graduate degree in genetics or genetic counseling.”
22-day-old cardiomyocytes that Madeline differentiated.
Stem Cell Internship: Stem Cell Core, Gladstone Institutes
Project Title: Genome Engineering Using CRISPR Technology to Investigate SARS-CoV-2 Infection in Cardiomyocytes
Abstract: SARS-CoV-2 is a novel type of coronavirus that causes the respiratory disease known as COVID-19, which has had devastating effects on society for over a year. The SARS-CoV-2 virus utilizes a cell surface protein called ACE2 to infect cells. By binding to ACE2, SARS-CoV-2 is able to enter cells and use them to replicate. Although the virus first enters the body through the respiratory tract, heart damage has also been observed in many patients. Therefore it is critical to understand the role of ACE2 in heart cells as well. In one recent study conducted at Gladstone, three types of human iPSC-derived cardiac cells were deliberately infected with SARS-CoV-2. Only the cardiomyocytes expressed ACE2 and were actively infected, yet all three cell types sustained damage consistent with the damage seen in patients - fragmented cell bodies and dissociation from neighboring cells. To further research the exact mechanism of the damage, we have successfully generated three isogenic ACE2 knockout lines from iPSCs using CRISPR/Cas9. Our next steps will be to differentiate these lines into cardiomyocytes and compare the levels of ACE2 expression. Eventually, they will be used in virology studies and infected with live SARS-CoV-2.