Key result
PSGL-1 deficiency reduces monocyte infiltration, attenuating neointima and plaque formation in atherosclerosis-prone mice.
Why the study?
The mechanism by which Ly-6Chi monocytes selectively accumulate in atherosclerotic lesions in mice is largely unknown, particularly the role of PSGL-1 in their homing.
Population
Wild-type, ApoE(-/-), and ApoE(-/-)/PSGL-1(-/-) mice
Comparison
ApoE(-/-)/PSGL-1(-/-) mice vs ApoE(-/-) mice with intact PSGL-1
Design
Preclinical experimental study in mice
Authors
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PSGL-1 may be a target to limit monocyte-driven plaque progression; extends murine mechanisms but leaves human translation open.
PSGL-1 mediates the preferential homing of Ly-6Chi monocytes to atherosclerotic lesions, and its deletion reduces plaque size and neointima formation in mice.
An et al. (2008) studied Atherosclerosis. PSGL-1 deficiency vs. Intact PSGL-1 (ApoE(-/-) mice) was evaluated on Monocyte recruitment to atherosclerotic lesions and neointima formation. PSGL-1 deficiency in ApoE(-/-) mice significantly reduced Ly-6Chi monocyte infiltration and resulted in smaller neointima and atherosclerotic plaques compared to mice with intact PSGL-1.
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