Discipline: Biological Sciences
Room: Exhibit Hall A
Carolynn Gonzalez - Truman State University
Co-Author(s): Monica Chang-Panesso, MD, Benjamin Humphreys, MD, PhD, Washington University School of Medicine, St. Louis, MO
Acute kidney injury (AKI) is the rapid degeneration of kidney function and increases the risk for chronic kidney disease (CKD). Chronic kidney disease leads to kidney failure. The only solutions to kidney failure are receiving a transplant and/or undergoing dialysis. As a result, understanding the mechanisms behind repair after injury can lead to prevention efforts for chronic kidney disease and better care following injury. When injury occurs, epithelial cells have been shown to dedifferentiate, proliferate, and redifferentiate to complete repair. If the kidney fails to repair, this leads to fibrosis ? the scarring of injured tissue. Foxm1 was identified as a transcription factor regulating proliferation of human proximal tubular epithelial cells in vitro, suggesting it might have a role in tubular epithelial repair. With this knowledge, we want to know if knocking out Foxm1 in vivo will reduce tubular epithelial proliferation after renal injury. We are also interested in knowing the long-term effects of Foxm1 deletion and if it will lead to fibrosis. We used a mouse model that allows genetic deletion of Foxm1 in all cells. After inducing ischemic injury in the kidney, we collected the kidneys and performed downstream analysis evaluating for proliferation and fibrosis using qPCR data and immunofluorescent tissue staining. Our control mice lacked ischemic injury. We were able to determine that deletion of Foxm1 inhibits proliferation in vivo, making it a necessary transcription factor for repair. We were unable to conclusively determine the long-term effects of Foxm1 deletion and hope to further explore this in the future.
Funder Acknowledgement(s): I would like to gratefully acknowledge the financial and professional support of the National Science Foundation under the Missouri Louis Stokes Alliance for Minority Participation, Award No. 1619639.
Faculty Advisor: Dr. Monica Chang-Panesso, firstname.lastname@example.org
Role: I conducted all parts of this research, excluding the mice surgery in which ischemic injury was induced, though I did observe the procedure. I executed qPCR and analyzed this data with the assistance of my mentor. Following qPCR, I used a cryostat tissue sectioner to section mice kidney tissue and then proceeded to stain it for immunofluorescent analysis. I observed these stained tissues under a confocal microscope, took photos, and then hand-counted the cells in these photos.