Related Experiment Video

Updated: Jul 10, 2026

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
09:57

Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages

Published on: August 12, 2019

Attenuation of monocyte chemoattractant protein-1 expression via inhibition of nuclear factor-kappaB activity in

Xinyu Gao1, Masaru Iwai, Shinji Inaba

  • 1Department of Molecular Cardiovascular Biology and Pharmacology, Ehime University Graduate School of Medicine, Shitsukawa, Tohon, Ehime, Japan.

American Journal of Hypertension
|October 24, 2007
PubMed
Abstract

Insights

Nifedipine, a calcium channel blocker, reduces monocyte chemoattractant protein-1 (MCP-1) expression in vascular injury by inhibiting nuclear factor-kappaB (NF-kappaB) activation, improving vascular remodeling.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Inflammation Research

Background:

  • Inflammatory vascular injury involves monocyte chemoattractant protein (MCP)-1.
  • Nuclear factor (NF)-kappaB plays a role in regulating MCP-1 expression.

Purpose of the Study:

  • To investigate the effect of a calcium channel blocker (CCB) on MCP-1 expression in inflammatory vascular injury.
  • To elucidate the role of NF-kappaB in CCB-mediated regulation of MCP-1.

Main Methods:

  • Vascular injury induced by cuff placement in mice.
  • MCP-1 expression analyzed by real-time RT-PCR.
  • NF-kappaB and IkappaB expression/activity assessed by Western blot and electrophoretic mobility shift assay.

Main Results:

  • Cuff placement increased MCP-1, vascular smooth muscle cell proliferation, and neointimal formation.
  • NF-kappaB translocated to the nucleus and increased DNA-binding activity to the MCP-1 promoter.
  • Nifedipine treatment reduced vascular remodeling, MCP-1 expression, and NF-kappaB activation without altering blood pressure.

Conclusions:

  • MCP-1 expression in vascular injury is regulated by NF-kappaB activation.
  • Nifedipine inhibits NF-kappaB nuclear translocation and DNA-binding activity, reducing MCP-1 expression and improving vascular remodeling.

More Related Videos

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment10:59

Conditional Knockdown of Gene Expression in Cancer Cell Lines to Study the Recruitment of Monocytes/Macrophages to the Tumor Microenvironment

Published on: November 23, 2017

Related Concept Videos

Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Inflammation01:38

Inflammation

Overview
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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 heterodimer of NF-κB...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...