Related Experiment Video

Updated: Jul 29, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
10:07

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

67.1K

lnc-MRGPRF-6:1 Promotes M1 Polarization of Macrophage and Inflammatory Response through the TLR4-MyD88-MAPK Pathway

Dan Hu1, Yuzhong Wang2, Zhihuan You1

  • 1Department of Cardiology, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing 210000, China.

Mediators of Inflammation
|February 7, 2022
PubMed
Abstract

Insights

Long noncoding RNA MRGPRF-6:1 (lnc-MRGPRF-6:1) promotes atherosclerosis by driving M1 macrophage polarization and inflammation. Inhibiting lnc-MRGPRF-6:1 reduces foam cell formation and inflammatory responses.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cardiovascular Research

Background:

  • Macrophage-driven inflammation is central to atherosclerosis (AS) pathogenesis.
  • Long noncoding RNAs (lncRNAs) are key regulators in inflammatory processes.
  • lnc-MRGPRF-6:1 was found upregulated in plasma exosomes of coronary atherosclerotic disease (CAD) patients.

Purpose of the Study:

  • To investigate the role of lnc-MRGPRF-6:1 in macrophage-mediated inflammation in AS.
  • To elucidate the molecular mechanisms underlying lnc-MRGPRF-6:1's function in AS.

Main Methods:

  • Correlation analysis of lnc-MRGPRF-6:1 with inflammatory factors in CAD patient plasma exosomes.
  • CRISPR/Cas9-mediated knockout of lnc-MRGPRF-6:1 in macrophages.
  • Assessment of macrophage polarization and foam cell formation.
  • RNA sequencing for transcriptome-wide analysis.

Main Results:

  • lnc-MRGPRF-6:1 expression is elevated in CAD patient exosomes and correlates with inflammatory cytokines.
  • lnc-MRGPRF-6:1 inhibition significantly reduces foam cell formation.
  • lnc-MRGPRF-6:1 knockout decreases M1 macrophage polarization.
  • lnc-MRGPRF-6:1 regulates macrophage polarization via the TLR4-MyD88-MAPK pathway.

Conclusions:

  • lnc-MRGPRF-6:1 knockdown inhibits M1 macrophage polarization and inflammatory response.
  • The TLR4-MyD88-MAPK signaling pathway is implicated in lnc-MRGPRF-6:1's regulatory role.
  • lnc-MRGPRF-6:1 is a critical regulator in the macrophage-mediated inflammatory process of AS.

More Related Videos

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line06:38

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line

Published on: August 2, 2021

29.3K
Reprograming Model of Human Monocyte-derived Macrophages for In-vitro Assays08:37

Reprograming Model of Human Monocyte-derived Macrophages for In-vitro Assays

Published on: April 18, 2025

590

Related Concept Videos

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...
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,...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...