Related Experiment Video

Updated: Feb 22, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.8K

Whole body and hematopoietic ADAM8 deficiency does not influence advanced atherosclerotic lesion development, despite

Kosta Theodorou1, Emiel P C van der Vorst1,2, Marion J Gijbels1,3,4

  • 1Department of Pathology, CARIM, Maastricht University, Maastricht, The Netherlands.

Scientific Reports
|September 17, 2017
PubMed

Insights

A Disintegrin And Metalloproteinase 8 (ADAM8) is upregulated in vulnerable atherosclerotic lesions. However, ADAM8 deficiency did not impact plaque development in mice, suggesting it may serve as a diagnostic biomarker.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Molecular Biology

Background:

  • A Disintegrin And Metalloproteinase 8 (ADAM8) is linked to inflammatory diseases and atherosclerosis.
  • Its specific role in the causal development of atherosclerosis remains uninvestigated.
  • ADAM8 influences immune cell recruitment and activation.

Purpose of the Study:

  • To investigate the expression and functional role of ADAM8 in human and mouse atherosclerosis.
  • To determine if ADAM8 deficiency affects the development and morphology of atherosclerotic plaques.

Main Methods:

  • Examined ADAM8 expression in human atherosclerotic lesions (early and progressed).
  • Assessed Adam8 expression in circulating immune cells (neutrophils, macrophages) in mice.
  • Utilized ADAM8-deficient mice (hematopoietic and whole-body) to study atherosclerosis development.

Main Results:

  • ADAM8 was significantly upregulated in vulnerable human atherosclerotic lesions, particularly in foam cell-rich shoulder regions.
  • ADAM8 was highly expressed in mouse neutrophils and macrophages; its deficiency reduced inflammatory mediator secretion.
  • Neither hematopoietic nor whole-body ADAM8 deficiency altered atherosclerotic lesion size or morphology in female mice, except for increased granulocytes.

Conclusions:

  • Whole-body and hematopoietic ADAM8 do not significantly contribute to advanced atherosclerotic plaque development in female mice.
  • ADAM8 expression may serve as a valuable diagnostic or prognostic biomarker for distinguishing stable from unstable atherosclerotic lesions.

More Related Videos

Quantification of Atherosclerosis in Mice06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

40.6K
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.6K

Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
1.5K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
695
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
443
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
476
Inflammation01:38

Inflammation

Overview
62.7K
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
605