Lung Repair – UROP Spring Symposium 2022

Lung Repair

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Kendall Foster

Pronouns: she/her

Research Mentor(s): Rachel Zemans
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 6 – 4:40pm – 5:30 pm
Room: League Ballroom
Authors:
Presenter: 94

Abstract

There are many chronic lung diseases that can occur because of the inability of the alveolar epithelium to regenerate after injury. The alveolar epithelium contains both Type 1 and Type 2 cells. After injury, Type 1 cells are more likely to die as opposed to Type 2 cells. The Type 2 cells that remain after injury are left to regenerate into Type 1 cells. Type 2 cells proliferate, then enter a transitional state in which cells either remain in that state and cause scarring (fibrosis) or return to normal and create new Type 1 cells. However, it is unknown why in fibrosis cells remain in this transitional state. We are conducting research to determine the role that various proteins have in the process of lung repair, and analyzing how we can employ this in finding remedies for diseases such as pulmonary fibrosis. We hypothesize that cells remain in this transitional state because they are senescent. To determine if transitional cells in fibrosis are senescent, we stained fibrotic mouse lungs with an antibody against p21, a marker of cell senescence, and K8, a marker of the transitional cells. After staining, we used a microscope to make images of the tissue. We found that transitional cells express p21, suggesting that they are senescent. We hope to continue discovering what factors both encourage and impair cell regeneration and use this to find therapies that advance cell regeneration.

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Interdisciplinary, Natural/Life Sciences

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