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FoxO4 inhibits atherosclerosis through its function in bone marrow derived cells.

Min Zhu¹, Qing-Jun Zhang, Lin Wang

¹Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Atherosclerosis

|October 19, 2011

Summary

FoxO4 deficiency in bone marrow cells exacerbates atherosclerosis by increasing inflammation and oxidative stress. This study reveals FoxO4

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Area of Science:

Cardiovascular Biology
Molecular Biology
Immunology

Background:

FoxO proteins regulate critical cellular functions like immune homeostasis and oxidative stress response.
Their role in atherosclerosis development remains largely unexplored.
FoxO4 is a key member of the FoxO family.

Purpose of the Study:

To investigate the role of FoxO4 inactivation in promoting atherosclerosis.
To determine if FoxO4 deficiency in vivo impacts atherosclerotic plaque development.

Main Methods:

Crossbreeding apolipoprotein E-deficient (apoE(-/-)) mice with Foxo4-deficient (Foxo4(-/-)) mice.
High-fat diet (HFD) induction and analysis of atherosclerotic lesions.
Bone marrow transplantation experiments in chimeric mice.
In vitro studies on macrophage inflammatory responses and reactive oxygen species (ROS) production.

Main Results:

Foxo4(-/-)apoE(-/-) mice exhibited significantly elevated atherosclerosis compared to apoE(-/-) controls after HFD.
Increased macrophage and T cell infiltration was observed in atherosclerotic plaques of Foxo4-deficient mice.
Foxo4-deficient bone marrow cells promoted atherosclerosis, and Foxo4-null macrophages showed heightened IL-6 and ROS production in vitro.
Serum IL-6 levels were upregulated in HFD-fed Foxo4(-/-)apoE(-/-) mice.

Conclusions:

FoxO4 acts as an inhibitor of atherosclerosis development.
Its inhibitory effect is mediated through bone marrow-derived cells.
FoxO4 may suppress atherosclerosis by reducing ROS and inflammatory cytokines, thereby limiting monocyte recruitment and retention.