What question did this study set out to answer?

To examine the expression and cellular localization of endothelin-converting enzyme-1 in rat carotid arteries after balloon injury and in human coronary atherosclerotic lesions.

January 7, 1997Circulation

Endothelin-Converting Enzyme Expression in the Rat Vascular Injury Model and Human Coronary Atherosclerosis

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Why the study?

Does ECE-1 blockade with phosphoramidon reduce neointimal formation in a rat vascular injury model?

Population

Rat carotid arteries after balloon injury and human coronary atherosclerotic lesions

Design

Preclinical

Follow-up

Up to 14 days

Authors

TMTohru MinaminoGeneral Cardiology HKHiroki KuriharaCross-Cutting Cardiology MTMasaaki TakahashiNational Institute for Environmental Studies

Discussion

Member takes

Implication

May support ECE-1 blockade for restenosis prevention; leaves open translation from this animal model to humans.

Key Points

To examine the expression and cellular localization of endothelin-converting enzyme-1 in rat carotid arteries after balloon injury and in human coronary atherosclerotic lesions.
Measured ECE-1 mRNA levels, ECE activity, and endothelin 1 content, and performed immunohistochemistry at 2 to 14 days after carotid balloon injury in rats treated with or without phosphoramidon.
Conducted immunohistochemical analysis of human coronary atherosclerotic lesions using smooth muscle alpha-actin and CD68 markers to determine the cellular distribution of ECE-1.
ECE-1 mRNA and enzymatic activity increased between 2 and 5 days after balloon denudation in rats, accompanied by increased tissue endothelin 1 and localization to neointimal smooth muscle cells by 5 to 14 days.
Phosphoramidon treatment effectively reduced neointimal lesion size following arterial balloon injury in rats.
Human coronary atheromatous plaques exhibited intense ECE-1 immunoreactivity localized specifically within smooth muscle cells and CD68-positive macrophages.

Structured PICO

Does ECE-1 blockade with phosphoramidon reduce neointimal formation in a rat vascular injury model?

Population

Rat carotid arteries after balloon injury and human coronary atherosclerotic lesions

Intervention

Phosphoramidon (inhibitor of neutral metalloproteases, including ECE-1)

Outcome

ECE-1 expression, localization, and size of neointimasurrogate

ECE-1 contributes to injury-induced neointimal formation and atherosclerosis, and its blockade may offer a therapeutic target for preventing restenosis.

Cite This Study

Minamino et al. (1997) studied this question.

synapsesocial.com/papers/6a779436a7498e5110aeabfa https://doi.org/10.1161/01.cir.95.1.221

Topics

Coronary artery disease Coronary CT angiography

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Endothelin-Converting Enzyme Expression in the Rat Vascular Injury Model and Human Coronary Atherosclerosis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Endothelin-Converting Enzyme Expression in the Rat Vascular Injury Model and Human Coronary Atherosclerosis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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