Fatty acid binding protein 3 deficiency limits atherosclerosis development via macrophage foam cell formation inhibition

Journal Article · Fri Oct 15 04:00:00 EDT 2021 · Experimental Cell Research

DOI:https://doi.org/10.1016/J.YEXCR.2021.112768· OSTI ID:23195500

Tan, Lili ^[1]; Lu, Jie; Liu, Limin; Li, Lu ^[2]

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1. Department of Cardiology, The Central Hospital Affiliated to Shenyang Medical College, Shenyang, Liaoning, People’s Republic of (China)
2. Department of Cardiology, The Second Affiliated Hospital of Shenyang Medical College, Shenyang, Liaoning, People’s Republic of (China)

Highlights: • We firstly indicated that FABP3 was highly expressed in the aorta of HFD-fed ApoE{sup −/-} mice. • Silencing FABP3 attenuated atherosclerosis due to inhibited macrophage foam cell formation. • FABP3 knockdown decreased foamy macrophage formation partly by inhibiting the PPARγ signal pathway. Atherosclerosis is the underlying contributing factor of cardiovascular disease, which is a process of inflammation and lipid-rich lesion. Macrophage-derived foam cell is a key hallmark of atherosclerosis and connected with various factors of lipid metabolism. Here, we showed that fatty acid binding protein 3 (FABP3) was upregulated in the aorta of ApoE{sup −/-} mice with high-fat-diet (HFD) feeding. Knockdown of FABP3 in HFD-fed ApoE{sup −/-} mice notably facilitated cholesterol efflux, inhibited macrophage foam cell formation, and thus prevented atherogenesis. Furthermore, FABP3 silencing decreased the expression of peroxisome proliferator-activated receptor γ (PPARγ). Mechanistic studies had disclosed the involvement of PPARγ signaling in balancing cholesterol uptake and efflux and diminishing foam cell formation. These findings firstly revealed an anti-atherogenic role of FABP3 silencing in preventing foamy macrophage formation partly through PPARγ, which might be a beneficial approach for therapying atherosclerosis.

• OSTI ID: 23195500
• Journal Information: Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 1 Vol. 407; ISSN 0014-4827; ISSN ECREAL
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
AORTA
ARTERIOSCLEROSIS
CARBOXYLIC ACIDS
CHOLESTEROL
INFLAMMATION
INHIBITION
LIPIDS
MACROPHAGES
METABOLISM
MICE
RECEPTORS
THERAPY
UPTAKE