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Extracellular NAD is a regulator for FcγR-mediated phagocytosis in murine macrophages
- Extracellular NAD is a regulator for FcγR-mediated phagocytosis in murine macrophages
- Song E.-K.; Lee Y.-R.; Yu H.-N.; Kim U.-H.; Rah S.-Y.; Park K.-H.; Shim I.-K.; Lee S.-J.; Park Y.-M.; Chung W.-G.; Kim J.-S.; Han M.-K.
- Ewha Authors
- 이승진; 심인경
- SCOPUS Author ID
- Issue Date
- Journal Title
- Biochemical and Biophysical Research Communications
- Biochemical and Biophysical Research Communications vol. 367, no. 1, pp. 156 - 161
- SCI; SCIE; SCOPUS
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- NAD is available in the extracellular environment and elicits immune modulation such as T cell apoptosis by being used as the substrate of cell surface ADP-ribosyl transferase. However, it is unclear whether extracellular NAD affects function of macrophages expressing cell surface ADP-ribosyl transferase. Here we show that extracellular NAD enhances Fcγ receptor (FcγR)-mediated phagocytosis in J774A.1 macrophages via the conversion into cyclic ADP-ribose (cADPR), a potent calcium mobilizer, by CD38, an ADP-ribosyl cyclase. Extracellular NAD increased the phagocytosis of IgG-coated sheep red blood cells (IgG-SRBC) in J774A.1 macrophages, which was completely abolished by pretreatment of 8-bromo-cADPR, an antagonist of cADPR, or CD38 knockdown. Extracellular NAD increased basal intracellular Ca2+ concentration, which also was abolished by pretreatment of 8-bromo-cADPR or CD38 knockdown. Moreover, the chelation of intracellular calcium abolished NAD-induced enhancement of phagocytosis of IgG-SRBC. Our results suggest that extracellular NAD act as a regulator for FcγR-mediated phagocytosis in macrophages. © 2007 Elsevier Inc. All rights reserved.
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