# Specific Beta-tubulin Isotype Involvement in Foam Cell Formation and Progression of Atherosclerosis

> **NIH NIH SC2** · ST. MARY'S UNIVERSITY · 2020 · $135,000

## Abstract

Project Summary/Abstract
Atherosclerotic cardiovascular disease is the leading cause of morbidity and mortality worldwide. Current
treatments for atherosclerosis focus on prevention or vessel repair with very few targeting the cellular events
leading to the progression of atherosclerosis. At the cellular level, the main effector cell of atherosclerosis is the
foam cell which is formed when macrophages undergo a morphological change associated with engulfment of
lipids. This is facilitated by the cytoskeleton which plays important roles in cell shape and function. Important
components of the cytoskeleton are the tubular polymers formed by the polymerization of dimers of α- and β-
tubulin called microtubules. The stability, dynamic properties, and behavior of a microtubule depend on the
composition of β-tubulin isotypes, of which there are many. The expression of these individual β-tubulin isotypes
can differ greatly across cell or tissue type. We hypothesize that a specific subset of β-tubulin isotypes regulates
foam cell formation and function. To understand the role of β-tubulin isotypes in foam cell formation and function,
we propose a comprehensive approach integrating in vitro and animal models to gain an understanding of the
biologically relevant roles β-tubulin isotypes play in foam cell formation and the development of atherosclerotic
plaques. We aim to establish the expression, distribution, and role of individual β-tubulins during foam cell
formation in vitro using primary cells (bone-marrow derived macrophage) and to determine the mechanism of β-
tubulin-dependent foam cell formation in vivo using mouse models of atherosclerosis. β-tubulin isotype levels
and cellular distribution will be measured in primary cells undergoing foam cell formation and within aortic lesions
using β-tubulin isotype-specific antibodies. β-tubulin gene expression will be quantified in cells and aortic tissue
using qRT-PCR. In addition, the effect that altering individual β-tubulin isotypes in primary cells or, with β-tubulin
binding drugs in mice, has on foam cells will be assessed. The proposed study will define the specific β-tubulin
isotypes involved in foam cell formation. Knowledge that we will gain could be used to design specific drugs that
inhibit foam cell formation, and subsequent plaque formation, by targeting specific β-tubulin isotypes.

## Key facts

- **NIH application ID:** 9925793
- **Project number:** 5SC2GM122611-03
- **Recipient organization:** ST. MARY'S UNIVERSITY
- **Principal Investigator:** Veronica E Contreras-Shannon
- **Activity code:** SC2 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $135,000
- **Award type:** 5
- **Project period:** 2018-07-09 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9925793

## Citation

> US National Institutes of Health, RePORTER application 9925793, Specific Beta-tubulin Isotype Involvement in Foam Cell Formation and Progression of Atherosclerosis (5SC2GM122611-03). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/9925793. Licensed CC0.

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