Related Experiment Video

Updated: Feb 9, 2026

Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model
05:35

Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model

Published on: August 25, 2020

11.8K

Apoptotic cell induction of miR-10b in macrophages contributes to advanced atherosclerosis progression in ApoE-/-

Dongliang Wang1,2, Wenting Wang1, Weiqun Lin1

  • 1Department of Nutrition, School of Public Health, Sun Yat-sen University, 74 Zhongshan Road II, Guangzhou, PR China.

Cardiovascular Research
|June 1, 2018
PubMed
Abstract

Insights

Macrophage miR-10b, induced by apoptotic cells, promotes advanced atherosclerosis by inhibiting cholesterol efflux. Inhibiting miR-10b with antagomiR-10b reduces plaque size and improves stability in ApoE-/- mice.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Immunology

Background:

  • MicroRNA-10b (miR-10b) previously shown to inhibit cholesterol efflux by repressing ATP binding cassette transporter A1 (ABCA1) in macrophages.
  • Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.

Purpose of the Study:

  • To elucidate the mechanism of macrophage miR-10b expression.
  • To investigate the role of miR-10b in the progression of atherosclerosis.

Main Methods:

  • Assessed miR-10b expression in atherosclerotic arteries of ApoE-/- mice.
  • Investigated miR-10b induction by free cholesterol-induced macrophage apoptotic cells (FC-AM) in resident peritoneal macrophages (RPM).
  • Utilized antagomiR-10b to inhibit miR-10b function in vitro and in vivo in ApoE-/- mice.

Main Results:

  • miR-10b expression increased in advanced atherosclerotic plaques.
  • FC-AM promoted miR-10b expression in RPM via Twist1/2 and Mer receptor tyrosine kinase.
  • AntagomiR-10b de-repressed ABCA1, enhanced reverse cholesterol transport, reduced plaque size, and improved plaque stability in advanced atherosclerosis.
  • miR-10b levels were critical for repressing ABCA1 in FC-AM-engulfing RPM.

Conclusions:

  • Apoptotic cell-induced miR-10b in macrophages is a key driver of advanced atherosclerosis.
  • Targeting miR-10b offers a potential therapeutic strategy for advanced atherosclerosis.

More Related Videos

Experimental Analysis of Apoptotic Thymocyte Engulfment by Macrophages06:47

Experimental Analysis of Apoptotic Thymocyte Engulfment by Macrophages

Published on: May 24, 2019

7.7K
Quantification of Atherosclerosis in Mice06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

40.4K

Related Concept Videos

Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized...
5.2K
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...
440
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...
1.1K
Binet's Contribution to Measures of Intelligence01:23

Binet's Contribution to Measures of Intelligence

Alfred Binet, along with his student Théophile Simon, was tasked by the French Ministry of Education in 1904 to create a method for identifying students who struggled to learn through conventional classroom instruction. This initiative aimed to address overcrowding by placing such students in specialized schools. Binet and Simon developed an intelligence test comprising 30 tasks, ranging from simple commands, like touching one's nose or ear, to more complex tasks, such as drawing...
1.8K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
8.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.7K