CLA-1/SR-BI is expressed in atherosclerotic lesion macrophages and regulated by activators of peroxisome proliferator-activated receptors
G Chinetti, FG Gbaguidi, S Griglio, Z Mallat… - Circulation, 2000 - Am Heart Assoc
G Chinetti, FG Gbaguidi, S Griglio, Z Mallat, M Antonucci, P Poulain, J Chapman…
Circulation, 2000•Am Heart AssocBackground—The scavenger receptors are cell-surface receptors for native and modified
lipoproteins that play a critical role in the accumulation of lipids by macrophages. CLA-1/SR-
BI binds HDL with high affinity and is involved in the cholesterol reverse-transport pathway.
Peroxisome proliferator–activated receptors (PPARs) are transcription factors regulating the
expression of genes implicated in lipid metabolism, cellular differentiation, and inflammation.
Here, we investigated the expression of CLA-1/SR-BI in macrophages and its regulation by …
lipoproteins that play a critical role in the accumulation of lipids by macrophages. CLA-1/SR-
BI binds HDL with high affinity and is involved in the cholesterol reverse-transport pathway.
Peroxisome proliferator–activated receptors (PPARs) are transcription factors regulating the
expression of genes implicated in lipid metabolism, cellular differentiation, and inflammation.
Here, we investigated the expression of CLA-1/SR-BI in macrophages and its regulation by …
Background—The scavenger receptors are cell-surface receptors for native and modified lipoproteins that play a critical role in the accumulation of lipids by macrophages. CLA-1/SR-BI binds HDL with high affinity and is involved in the cholesterol reverse-transport pathway. Peroxisome proliferator–activated receptors (PPARs) are transcription factors regulating the expression of genes implicated in lipid metabolism, cellular differentiation, and inflammation. Here, we investigated the expression of CLA-1/SR-BI in macrophages and its regulation by PPARs.
Methods and Results—CLA-1 is undetectable in human monocytes and is induced upon differentiation into macrophages. Immunohistological analysis on human atherosclerotic lesions showed high expression of CLA-1 in macrophages of the lipid core colocalizing with PPARα and PPARγ staining. Activation of PPARα and PPARγ resulted in the induction of CLA-1 protein expression in monocytes and in differentiated macrophages. Finally, SR-BI expression is increased in atherosclerotic lesions of apoE-null mice treated with either PPARγ or PPARα ligands.
Conclusions—Our data demonstrate that CLA-1/SR-BI is expressed in atherosclerotic lesion macrophages and induced by PPAR activation, identifying a potential role for PPARs in cholesterol homeostasis in atherosclerotic lesion macrophages.
Am Heart Assoc