ASCL3 in Vascular Biology: Cell Proliferation – UROP Spring Symposium 2022

ASCL3 in Vascular Biology: Cell Proliferation

photo of presenter

Zachary Rose

Pronouns: he/him

Research Mentor(s): Minerva Garcia-Barrio
Co-Presenter:
Research Mentor School/College/Department: Internal Medicine / Cardiovascular Center / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 3 – 1:40pm – 2:30 pm
Room: League Ballroom
Authors: Zachary Rose, Kathryn Kim, Minerva Garcia-Barrio
Presenter: 78

Abstract

Cardiovascular disease (CVD) remains a looming threat to human well-being; with 17.9 million lives claimed per year, it is the leading cause of death globally. Currently, CVD is managed through mitigating risk factors. This is accomplished through lifestyle changes such as maintaining a healthy weight and abstaining from smoking, or through medication to reduce cholesterol, improve blood flow, or regulate heart rhythm. At the root, CVD is a consequence of vascular dysfunction of the endothelium, vascular smooth muscle cells (VSMCs), or perivascular adipose tissue. This study targets VSMCs and their failure, which is due to increased proliferation, increased apoptosis, or reduced contractility. A screen for genes that increased proliferation in VSMCS was performed that found the Achaete Scute-like (ASCL) family expressed in these cells. The expression of ASCL genes, especially ASCL3, was a surprise because it was previously thought to be specific to salivary glands or cancers. Previous studies in the lab of the principal investigator showed that upregulation of ASCL3 increases proliferation and protects against apoptosis. We aim to understand the role of ASCL3 in VSMCs, hypothesizing that changes in ASCL3 levels will change the expression of key genes in the cell cycle. To do this, we first seek to characterize the expression of ASCL3 in relation to key genes in the cell cycle. We extracted mRNA from A7r5 cells at varying confluences, made cDNA, and performed qRT-PCR. Since ASCL3 is a transcription factor, we expect that changes in ASCL3 will indeed correlate with the expression of major genes in the cell cycle. Identifying new genes involved in the emergence of such deadly diseases, like ASCL3’s potential link to CVD, can lead to new targets of intervention.

Presentation link

Biomedical Sciences, Natural/Life Sciences, Natural/Life Sciences

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