Pooja Kapoor
Pronouns: she/her
Research Mentor(s): Jason Knight
Research Mentor School/College/Department: Internal Medicine/Rheumatology / Medicine
Program:
Authors: Chao Liu, Jason Knight
Session: Session 3: 11:00 am – 11: 50 am
Poster: 52
Abstract
According to the CDC’s National Diabetes Statistics Report (2020), an estimated 10.5% of the U.S. population has been diagnosed with diabetes. The same report noted that a remarkable 7.5% of diabetic patients are hospitalized with “major CVD” in a given year. Indeed, cardiovascular complications—especially myocardial infarction and stroke—are a primary driver of morbidity and mortality in type 1 and type 2 diabetes. The mechanisms underlying this increased cardiovascular risk are still poorly understood. In the previous paper of our lab, we reported that inhibition of neutrophil extracellular trap formation alleviates vascular dysfunction in type 1 diabetic mice. We also discovered in a single-cell RNA-seq experiment that the long non-coding RNA, Malat1, was significantly changed in diabetic aorta. In this project, the expression of Malat1 in different cell types of the aorta, including endothelial cells and smooth muscle cells, and the impact of neutrophil extracellular traps (NETs) was investigated. The single cell RNA-seq data was analyzed by our collaborator. Different human cell types, including human umbilical vein endothelial cells (HUVECs) and human aortic smooth muscle cells (HASMCs) with high-glucose and/or NETs, were treated and the RNA expressions of Malat1 were tested by real-time qPCR. We found that hyperglycemia significantly regulated Malat1 in HUVECs and HASMCs; and NETs have the similar effects. The combined effect of high glucose and NETs is in the process of being explored. Ultimately, we will reveal the expression of Malat1 in aortic cells and its relationship with NETs, leading to a better understanding of the mechanisms behind vascular dysfunction in diabetic patients.
