Related Experiment Video

Updated: Nov 22, 2025

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

8.4K

IRF-1 contributes to the pathological phenotype of VSMCs during atherogenesis by increasing CCL19 transcription

Yongbin Shen1, Zhanfeng Sun1, Shuran Mao2

  • 1Department of Vascular Surgery, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China.

Aging
|January 11, 2021
PubMed

Insights

Interferon regulatory factor 1 (IRF-1) drives atherosclerosis by increasing chemokine ligand 19 (CCL19) transcription, promoting vascular smooth muscle cell dysfunction and inflammation.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis (AS) is a chronic inflammatory arterial disease with incompletely understood mechanisms.
  • Chemokine ligand 19 (CCL19) is upregulated in AS patients, but its role remains unclear.

Purpose of the Study:

  • To elucidate the role of CCL19 in AS pathogenesis.
  • To investigate the regulatory mechanism of CCL19 expression in AS.

Main Methods:

  • ELISA, immunohistochemistry (IHC), quantitative reverse transcription PCR (QRT-PCR), and Western blot were used to assess CCL19 levels.
  • Chromatin immunoprecipitation (ChIP) and luciferase assays identified IRF-1 as a transcriptional activator of CCL19.
  • Experiments involved cell culture (VSMCs) and a mouse model of high-fat-diet-induced AS.

Main Results:

  • CCL19 overexpression promoted inflammatory factor secretion, extracellular matrix deposition, and VSMC proliferation/migration.
  • CCL19 knockdown attenuated PDGF-BB-induced VSMC inflammation and matrix deposition.
  • IRF-1 activated CCL19 transcription; IRF-1 silencing inhibited AS progression, VSMC proliferation/migration, and CCL19 expression in mice.

Conclusions:

  • IRF-1 promotes VSMC pathological phenotypes during atherogenesis by upregulating CCL19 transcription.
  • Targeting the IRF-1/CCL19 axis may offer a therapeutic strategy for atherosclerosis.

Keywords:
CCL19IRF-1VSMCSatherosclerosis

More Related Videos

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

8.6K
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

14.2K

Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
556
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
9.2K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.1K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
8.8K
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...
188
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...
389