Maya Barnabas
Pronouns: she/her
Research Mentor(s): Jason Knight
Research Mentor School/College/Department: Internal Medicine/Rheumatology / Medicine
Program:
Authors: Chao Liu
Session: Session 3: 11:00 am – 11: 50 am
Poster: 53
Abstract
Diabetes is one of the leading causes of death in the United States due to its various complications such as cardiovascular issues, including vascular dysfunction and atherosclerosis which can lead to a heart attack or stroke. In the previous paper of our lab, we reported “inhibition of neutrophil extracellular trap formation alleviates vascular dysfunction in type 1 diabetic mice.” We now aim to discover whether or not there is a relationship between neutrophil extracellular traps (NETs) – infection-fighting white blood cells – and plaque formation in the AAV-PCSK9 induced atherosclerosis mice model. The 12-week-old diabetic Akita (AK) mice and Wild-Type (WT) mice were injected with AAV-PCSK9 and fed with a high-fat diet (HFD) that creates high lipid levels leading to atherosclerosis. Once the mice reached 12 weeks of the AAV-HFD treatment, they were sacrificed and their plasmas were collected. After the fixed mice aortas were cut and stained to depict any plaque build-up, pictures of the aorta were analyzed by software Image J. Compared to the WT-saline-HFD group, the WT-AAV-HFD group has a higher staining positive area per thoracic aorta area (~5%), which confirmed the success of the atherosclerosis model. The AK-AAV-HFD group has a significantly higher staining positive area (~3%) compared to the WT-AAV-HFD group. We are still testing the level of NETs in the plasma by the MPO-DNA assay. In conclusion, diabetic mice have an environment of high glucose that accelerates plaque formation in the aorta of an atherosclerosis mice model. These conclusions can eventually help find the potential target for cardiovascular diseases in diabetes patients.
