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Papers In Press, published online ahead of print November 19, 2004
Department of Biochemistry, Chonbuk National University Medical School, Chonju, Chonbuk 561-182
Corresponding Author: uhkim{at}moak.chonbuk.ac.kr
CD38 is a ADP-ribosyl cyclase, producing a potent Ca2+-mobilizer cyclic ADP-ribose (cADPR). In this study, we have investigated a role of CD38 and its regulation through IL8 signaling in lymphokine-activated killer (LAK) cells. Incubation of LAK cells with IL8 resulted in an increase of cellular cADPR level and a rapid rise of intracellular Ca2+ concentration ([Ca2+]i), which sustained for a long period of time (>10 min). Preincubation of an antagonistic cADPR analog, 8-Br-cADPR abolished the sustained Ca2+ signal only but not the initial Ca2+ rise. An IP3 receptor antagonist blocked both Ca2+ signals. Interestingly, the sustained Ca2+ rise was not observed in the absence of extracellular Ca2+. Functional CD38-null (CD38-) LAK cells showed the initial rapid increase of [Ca2+]i but not the sustained Ca2+ rise in response to IL8 treatment. An increase of cellular cADPR level by cGMP analog, 8-pCPT-cGMP but not cAMP analog or PMA was observed. IL8 treatment resulted in the increase of cGMP level that was inhibited by the IP3 receptor blocker but not a PKC inhibitor. cGMP-mediated Ca2+ rise was blocked by 8-Br-cADPR. In addition, IL8-mediated LAK cell migration was inhibited by 8-Br-cADPR and a PKG inhibitor. Consistent with these observations, IL8-induced migration of CD38- LAK cells was not observed. However, direct application of cADPR or 8-pCPT-cGMP stimulated migration of CD38- cells. These results demonstrate that CD38 is stimulated by sequential activation of IL8 receptor, IP3-mediated Ca2+ rise, and cGMP/PKG and that CD38 plays an essential role in IL8-induced migration of LAK cells.
J. Biol. Chem, 10.1074/jbc.M409592200
Submitted on August 20, 2004
Revised on November 19, 2004
Accepted on November 19, 2004
Activation of CD38 by IL8 signaling regulates intracellular Ca2+ level and motility of lymphokine-activated killer cells
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