Related Experiment Video

Updated: Oct 27, 2025

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
07:46

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation

Published on: April 3, 2017

25.6K

G protein-coupled receptor 39 activation alleviates oxidized low-density lipoprotein-induced macrophage inflammatory

Lu Chen1, Zhengdong Fang2, Xiaotian Wang2

  • 1Department of Vascular Surgery, Provincial Hospital Affiliated to Anhui Medical University, Hefei City, Anhui Province, China.

Bioengineered
|July 21, 2021
PubMed

Insights

Activating G protein-coupled receptor 39 (GPR39) protects macrophages from oxidized LDL damage. This occurs by increasing A20 expression, reducing inflammation, lipid buildup, and cell death, thereby combating atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Immunology

Background:

  • Atherosclerosis involves monocyte attachment to endothelial cells, driven by oxidized low-density lipoprotein (ox-LDL).
  • G protein-coupled receptor 39 (GPR39) is implicated in mitigating atherosclerosis, but its role in macrophage response to ox-LDL requires elucidation.

Purpose of the Study:

  • To investigate if GPR39 activation protects macrophages against ox-LDL-induced inflammation and apoptosis.
  • To explore the underlying mechanism, focusing on the role of tumor necrosis factor alpha-induced protein 3 (TNFAIP3, also known as A20).

Main Methods:

  • Assessed GPR39 and A20 expression in ox-LDL-treated Raw 264.7 cells using RT-qPCR and western blotting.
  • Evaluated macrophage viability, inflammation (cytokine levels, NF-κB, COX2), lipid accumulation (Oil Red O, cholesterol assays), and apoptosis (TUNEL, western blotting) with GPR39 agonist and A20 interference.

Main Results:

  • Ox-LDL reduced GPR39 and A20 expression in macrophages.
  • GPR39 agonist significantly upregulated A20 expression in ox-LDL-treated macrophages.
  • Interfering with A20 abolished the protective effects of the GPR39 agonist against ox-LDL-induced inflammation, lipid accumulation, and apoptosis.

Conclusions:

  • GPR39 activation mitigates ox-LDL-induced macrophage inflammation, lipid accumulation, and apoptosis.
  • This protective effect is mediated through the upregulation of A20, highlighting a novel therapeutic pathway for atherosclerosis.

Keywords:
A20AtherosclerosisGPR39inflammatory responsemacrophage

More Related Videos

LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring08:45

LDL Cholesterol Uptake Assay Using Live Cell Imaging Analysis with Cell Health Monitoring

Published on: November 17, 2018

13.7K
Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

3.2K

Related Concept Videos

Inflammation01:38

Inflammation

Overview
56.6K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
6.2K
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
6.9K
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...
4.1K
Receptor-mediated Endocytosis01:39

Receptor-mediated Endocytosis

Overview
107.9K
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
14.4K