Extracellular NAD is a regulator for FcγR-mediated phagocytosis in murine macrophages

Eun Kyung Song, Young Rae Lee, Hong Nu Yu, Uh Hyun Kim, So Young Rah, Kwang Hyun Park, In Kyung Shim, Seung Jin Lee, Yeong Min Park, Weon Guu Chung, Jong Suk Kim, Myung Kwan Han

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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.

Original languageEnglish
Pages (from-to)156-161
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
StatePublished - 29 Feb 2008

Bibliographical note

Funding Information:
This work was supported by grants of the Korea Science and Engineering Foundation (Nos. R01-2002-000-00493-0 and M10528010003-05N2801-00310) and the grant of Post-Doc Program, Chonbuk National University (E.-K. Song).


  • Cyclic ADP-ribose
  • Fcγ receptor
  • Macrophages
  • NAD
  • Phagocytosis


Dive into the research topics of 'Extracellular NAD is a regulator for FcγR-mediated phagocytosis in murine macrophages'. Together they form a unique fingerprint.

Cite this