Cole Weber
Pronouns: He/Him/His
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: Cole Weber, Rachel Zemans, Norihito Kaku
Presenter: 93
Abstract
When a lung’s alveolar epithelium is damaged, type 1 and type 2 alveolar epithelial are destroyed; however, any type 2 cells that remain regenerate into both type 1 and type 2 cells (Evans Am J Pathol 1973, Barkauskas JCI 2013). Yet, the lung’s repair function can be impaired, and type 1 cells aren’t regenerated from type 2 cells leading to scarring or permanent damage in the lungs. We aim to elucidate how genetic makeup, different immune cells, and proteins play into the function of host defense and lung repair and how we can manipulate these aspects to make the lung repair itself once again. This manipulation could lead to different therapies for diseases like fibrosis or pneumonia to lessen the death rate and negate the symptoms. Based on RNA sequencing (Riemondy JCI Insight 2019), we hypothesized that expression of protein Keratin 8 (K8) is increased in type 2 cells after lung injury. Immunofluorescence staining, microscopy, and image analysis software are employed to measure the intensity of K8 protein in mouse lungs. Through these tests, it has been discovered that the K8 protein has a significant presence in damaged lungs compared to undamaged lungs meaning K8 protein is key in lung injury and inflammation.
Interdisciplinary, Natural/Life Sciences
