What is the clinical evidence from this study?

Study design: Other. Population: Atherosclerosis. Intervention: PPARalpha and PPARgamma ligands. Primary outcome: CLA-1/SR-BI expression in macrophages.

What does this research mean for the field?

Activation of PPARalpha and PPARgamma induces CLA-1/SR-BI expression in monocytes, differentiated macrophages, and atherosclerotic lesions. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To investigate CLA-1/SR-BI expression in macrophages and evaluate its regulation by peroxisome proliferator-activated receptors (PPARs).

May 23, 2000Circulation

CLA-1/SR-BI Is Expressed in Atherosclerotic Lesion Macrophages and Regulated by Activators of Peroxisome Proliferator-Activated Receptors

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Key result

Activating PPARalpha and PPARgamma induces CLA-1/SR-BI expression in human macrophages and murine atherosclerotic lesions.

Why the study?

The role and regulation of CLA-1/SR-BI expression in macrophages within atherosclerotic lesions and its modulation by PPAR activators were not fully understood.

Does PPAR activation increase CLA-1/SR-BI expression in macrophages and atherosclerotic lesions?

Population

Human monocytes and macrophages, human atherosclerotic lesions, and apoE-null mice

Comparison

PPARalpha and PPARgamma ligand treatment vs no treatment

Design

Preclinical experimental study

Authors

GCGiulia ChinettiInserm FGF. GbaguidiInserm SGS. GriglioInserm

Discussion

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Implication

Hypothesis-generating for PPAR agonists in plaque cholesterol homeostasis; leaves open translation to human atherosclerosis therapy.

Key Points

To investigate CLA-1/SR-BI expression in macrophages and evaluate its regulation by peroxisome proliferator-activated receptors (PPARs).
Assessed CLA-1 expression during monocyte-to-macrophage differentiation and performed immunohistochemical analyses of human atherosclerotic lesions.
Treated human monocytes and differentiated macrophages with PPARalpha and PPARgamma ligands to evaluate CLA-1 protein induction.
Administered PPARalpha or PPARgamma ligands to apoE-null mice to assess SR-BI expression in vivo within atherosclerotic plaques.
CLA-1 was undetectable in circulating monocytes but was markedly induced upon differentiation into macrophages, colocalizing with PPARalpha and PPARgamma in the lipid core of human atherosclerotic lesions.
Activation of PPARalpha and PPARgamma induced CLA-1 protein expression in both monocytes and differentiated macrophages.
Treatment of apoE-null mice with PPARalpha or PPARgamma agonists increased SR-BI expression in atherosclerotic plaques.

Structured PICO

Does PPAR activation increase CLA-1/SR-BI expression in macrophages and atherosclerotic lesions?

Population

Human monocytes/macrophages, human atherosclerotic lesions, and apoE-null mice

Exposure

PPARgamma or PPARalpha ligands

Outcome

Expression of CLA-1/SR-BI proteinsurrogate

PPAR activation induces CLA-1/SR-BI expression in macrophages, suggesting a role for PPARs in cholesterol homeostasis within atherosclerotic lesions.

Cite This Study

Chinetti et al. (2000) studied Atherosclerosis. PPARalpha and PPARgamma ligands was evaluated on CLA-1/SR-BI expression in macrophages. Activation of PPARalpha and PPARgamma induced CLA-1/SR-BI expression in human monocytes/macrophages and in atherosclerotic lesions of apoE-null mice.

synapsesocial.com/papers/6a09f8a616dfdfe7ed3484d2 https://doi.org/10.1161/01.cir.101.20.2411

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CLA-1/SR-BI Is Expressed in Atherosclerotic Lesion Macrophages and Regulated by Activators of Peroxisome Proliferator-Activated Receptors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

CLA-1/SR-BI Is Expressed in Atherosclerotic Lesion Macrophages and Regulated by Activators of Peroxisome Proliferator-Activated Receptors

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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