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Ecto-5'-nucleotidase/CD73 reduces COX-2 expression in activated macrophages
Md Mostafizur Rahman1, Anuvrat Sircar1, Simran Lakhina1
1Neuroinflammation Research Lab, Faculty of Life Sciences and Biotechnology, South Asian University, Rajpur Road, Maidan Garhi, New Delhi, 110068, India.
Scientific Reports
|January 4, 2026
Summary
Overexpression of ecto-5'-nucleotidase (CD73) in macrophages reduces inflammation by decreasing cyclooxygenase 2 (COX-2) expression. This modulation occurs through increased adenosine formation, impacting the NF-κB pathway.
Area of Science:
- Immunology
- Biochemistry
Background:
- Extracellular ATP (eATP) promotes inflammation via cyclooxygenase 2 (COX-2) upregulation.
- Ectonucleotidases, like ecto-5 -nucleotidase (CD73), hydrolyze AMP to adenosine, potentially modulating inflammatory responses.
Purpose of the Study:
- To investigate if CD73 overexpression can modulate COX-2 expression in macrophages.
- To explore the mechanism by which CD73 affects COX-2 levels.
Main Methods:
- CD73 was expressed in bacterial and mammalian systems.
- J774A.1 macrophage cells were treated with recombinant CD73 or transfected with CD73, then co-stimulated with LPS and AMP.
- COX-2 expression and CD73 activity (inorganic phosphate release) were measured.
Main Results:
- Exogenous and transfected CD73 reduced COX-2 expression in LPS-activated macrophages stimulated with ATP or AMP.
- The inhibitory effect of CD73 on COX-2 was abolished by the CD73 inhibitor AMP-CP.
- The reduction in COX-2 expression was linked to the NF-κB pathway, not p42/44 MAPK.
Conclusions:
- CD73 overexpression effectively reduces inflammation by decreasing COX-2 expression in macrophages.
- Increased adenosine formation resulting from CD73 activity is the key mechanism underlying this anti-inflammatory effect.
