- Friday, December 2, 2022
- 2:00 PM–2:50 PM
- SB 010
Calvin students present research from their summer internships
Exploring the Role of AHR Activation in Bladder Cancer Models
Hyeon Jin Kim
Immune checkpoint inhibitor therapy was designed to reinvigorate immune cells to bind and kill cancer cells. However, the treatment that was intended to help patients resulted in hyper progressive disease (when the tumor shows accelerated growth, leading to an explosion of tumor growth in a short period of time). We searched for a particular gene that could function as a biomarker for hyper-progression. Upon inspecting tumor samples, we discovered a biomarker called CYP1A1. We thought to test if a tumor that expressed high levels of endogenous CYP1A1, treated with immunotherapy, ultimately led to hyper progression. Every step of the project was preliminary; thus, we did not have an experimental system to test the hypothesis. So, I helped develop the experimental system.
ER-Golgi vesicle trafficking in membrane repair in cardiomyocytes
Visakuo Tsurho
Loss of membrane repair due to genetic defects in the DYSF gene is associated with muscular dystrophies such as Miyoshi Myopathy and LGMD2B. Studies that have impeded membrane repair in skeletal muscle cells observe progressive muscle damage and muscle wasting, but membrane repair in cardiomyocytes. A predominant model for membrane repair is the patch hypothesis, which states that a calcium influx stimulates the movement of membranous structures to the injury site upon membrane injury. Lysosomes have been implicated to participate in membrane repair in non-muscle cells. However, the source of membranes and the molecular mechanisms involved in membrane repair in cardiomyocytes are unclear. The goal of this research was to identify the organelles and mechanisms in membrane repair in cardiomyocytes. We began by investigating lysosomes in human-induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs). Immunofluorescence staining for lysosomal protein LAMP-1 revealed much fewer LAMP-1 signals in hiPS-CMs than in non-CMs. Therefore, we considered the endoplasmic reticulum and Golgi as potential organelles involved in membrane repair. ER-Golgi protein, Sec22b, was used to investigate ER to Golgi vesicle trafficking in cardiomyocytes. hiPS-CMs were transfected with eGFP-Sec22b. We used ionomycin, an ionophore that increases intracellular calcium, to simulate the acute calcium rise following membrane injuries. After ionomycin treatment, eGFP-Sec22b did not significantly colocalize with cis-Golgi protein GM130. Our results suggest that a sharp global rise in intracellular calcium following membrane injuries may not effectively engage Sec22b targeting to the Golgi. However, a trend of greater Sec22b colocalization with GM130 after ionomycin treatment was observed which could be substantiated with more data. Hence, further studies would help understand the role of ER-Golgi vesicle trafficking in membrane repair in cardiomyocytes.
