Hello! My name is Gayatri Ratakonda and I’m a rising junior majoring in biology with minors in chemistry and English literature. I’m originally from New York, but chose to attend Pitt with the hopes of pursuing medical research at an institution with an established history of involving undergraduates in their work. I’m incredibly excited to be a part of the Brackenridge community of research scholars this year. Currently, I’m working at the Vascular Medical Institute at UPMC Presbyterian under the mentorship of Dr. Ruya Liu in the Gladwin Lab.
How the human body heals has always been a fascinating topic for researchers. From clotting small cuts to recovering broken bones, regeneration and repair after injury is what keeps us alive and functioning. While the mending of damaged tissue is both necessary and plentiful in many areas of our body, there are some cell types that cannot regenerate. Specifically, heart cells (cardiomyocytes) are unable to regrow after suffering any type of loss. Cardiomyocytes have a unique structure with multiple nuclei, making them much more complex. It is known that the maturing process of cardiomyocyte binucleation renders them unable to re-enter the cell cycle. This makes adult cardiomyocytes quiescent, meaning that they do not participate in active cell division. Not much is currently known about the proliferative potential of cardiomyocytes, or what can possibly induce their generation. A growing healthcare concern in America is heart disease which is characterized by arterial blockage. This led to over 659,000 deaths in the past year alone. As the trend shows no signs of slowing down, investigating ways to control the proliferation of cardiomyocytes has become incredibly important.
Our lab has been engaged in an effort to characterize the protein C5x and its role in controlling the cell cycle of cardiomyocytes. In the past, it has been observed that the absence of C5x has resulted in increased cell cycle activity, but a lower functional number of cardiomyocyte count overall in mice. We came to the conclusion that C5x must control an aspect of cell division, and therefore control the number of functional cardiomyocytes present in the heart. Our concern now is to figure out at which point of the cell cycle the cells are arresting at in the absence of C5x.
My current goal is to finish my undergraduate degree in biology and apply to medical school in the next cycle. I’m also interested in pursuing research in my future career, and have been considering the M.D. PhD. route in order to work towards my goal of becoming a physician scientist. However, the details are still constantly evolving!