Investigating the Function of CD36 in Hematopoietic Stem Cells – UROP Spring Symposium 2022

Investigating the Function of CD36 in Hematopoietic Stem Cells

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Timothy Liang

Pronouns: He/Him/His

Research Mentor(s): Qing Li
Co-Presenter:
Research Mentor School/College/Department: Medicine Division of Hematology & Oncology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 3 – 1:40pm – 2:30 pm
Room: League Ballroom
Authors: Timothy Liang, Qing Li, Morgan Jones
Presenter: 55

Abstract

Hematopoietic stem cells (HSCs) are blood-forming stem cells that regularly replenish mature blood within the body to allow for organism survival. These cells must also be able to detect and respond to different types of stress, such as infection, blood loss, and myeloablation. The mechanisms by which HSCs respond to stressors is still largely unknown, though metabolic alterations appear to be an integral part in such a proliferative system. CD36 is a protein of interest which is known to function in both inflammatory modulation and fatty acid uptake in other cells. Recent studies have also linked CD36 to facilitating fatty acid uptake in leukemic stem cells. Because of its multiple roles and significance in hematopoiesis, we wanted to ascertain if CD36 has a function in HSC proliferation and homeostasis. With wild-type mice expressing CD36 and genetically modified mice without CD36, it was determined that CD36 is not necessary for stable hematopoiesis under regular conditions. After evaluating mice given bone marrow transplants, it was found that the protein is not required for competitive fitness of HSCs either. However, the lack of CD36 provides protection to mice after sequential 5FU injections which cause myeloablative stress that tests the regenerative ability of the blood-forming system. This indicates that CD36 loss is protective under myeloablative conditions. Initial experiments have shown that the fatty acid transport role of CD36 is not involved in this observation, meaning that the inflammatory role may be harmful to HSC function. This development is currently being examined with an NFKB reporter in mice that can monitor inflammation in HSCs. These studies will provide novel insights into the function of CD36 in HSCs and give new information about the mechanisms by which stem cells fulfill proliferative demands under stress.

Presentation link

Interdisciplinary, Natural/Life Sciences

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