Related Experiment Video
Updated: May 24, 2026
11:29
HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
Published on: July 20, 2016
Regulation of macrophage function by adenosine
1Department of Surgery, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, 07103, USA. haskoge@umdnj.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|March 17, 2012
Summary
Adenosine, an endogenous nucleoside, modulates immune responses by targeting mononuclear phagocytes through four specific receptors. This regulation influences inflammation, vascular diseases, and cancer progression.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Adenosine is an endogenous nucleoside released during metabolic disturbances.
- Mononuclear phagocyte system cells are key targets of adenosine's immunomodulatory effects.
- Adenosine exerts its functions through four G-protein-coupled cell membrane receptors: A(1), A(2A), A(2B), and A(3).
Purpose of the Study:
- To elucidate the role of adenosine and its receptors in regulating mononuclear phagocyte functions.
- To understand how adenosine signaling impacts immune cell differentiation and activation.
- To explore adenosine's influence on angiogenesis and disease pathogenesis.
Main Methods:
- Analysis of adenosine's effects on osteoclast differentiation via A(1) receptors.
- Investigation of adenosine's impact on monocyte to dendritic cell differentiation via A(2B) receptors.
- Assessment of adenosine's regulation of classical and alternative macrophage activation through A(2A) and A(2B) receptors.
- Evaluation of adenosine-mediated induction of vascular endothelial growth factor (VEGF) production and its role in angiogenesis.
Main Results:
- Adenosine promotes osteoclast differentiation via A(1) receptors.
- Adenosine alters monocyte to dendritic cell differentiation through A(2B) receptors.
- Adenosine downregulates classical macrophage activation via A(2A) receptors and upregulates alternative activation via A(2B) receptors.
- Adenosine induces VEGF production by mononuclear phagocytes through A(2A), A(2B), and A(3) receptors, promoting angiogenesis.
Conclusions:
- Adenosine plays a critical role in modulating mononuclear phagocyte functions.
- Adenosine receptor signaling dictates immune cell differentiation, activation, and inflammatory responses.
- Adenosine's regulation of mononuclear phagocytes impacts the progression of inflammatory diseases, vascular conditions, and cancer.
Related Concept Videos
01:19Regulation of Metabolism
Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
01:28Global Regulatory Systems
Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...
01:09GPCRs 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 cells.
Two...
Two...
01:27Adrenergic Receptors (Adrenoceptors): Classification
Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
01:31Adrenergic Receptors: ɑ Subtype
Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
01:25Adrenergic Agonists: Indirect-Acting Agents
Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...