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Engulfment of Apoptotic Cells Locus-1 in a Subset of Macrophages for Expression of Developmental Endothelial Expression of Developmental Endothelial Locus-1 in a Subset of Macrophages for Engulfment of Apoptotic Cells This information is current as Rikinari Hanayama, Masato Tanaka, Keiko Miwa and of September 29, 2021. Shigekazu Nagata J Immunol 2004; 172:3876-3882; ; doi: 10.4049/jimmunol.172.6.3876 http://www.jimmunol.org/content/172/6/3876 Downloaded from References This article cites 49 articles, 16 of which you can access for free at: http://www.jimmunol.org/content/172/6/3876.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2004 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Expression of Developmental Endothelial Locus-1 in a Subset of Macrophages for Engulfment of Apoptotic Cells1 Rikinari Hanayama,* Masato Tanaka,*† Keiko Miwa,*‡ and Shigekazu Nagata2*‡§ A major function of macrophages is to engulf apoptotic cells to prevent them from releasing noxious materials as they die. Milk fat globule-EGF-factor 8 (MFG-E8) is a glycoprotein secreted by activated macrophages that works as a bridge between apoptotic cells and phagocytes by specifically recognizing phosphatidylserine exposed on apoptotic cells. In this study, we found that ␣ ␤ developmental endothelial locus-1 (Del-1), originally identified as an embryonic endothelial cell protein that binds v 3 integrin, is structurally and functionally homologous to MFG-E8. That is, both consist of a signal sequence, two epidermal growth factor domains and two factor VIII-homologous domains (C1 and C2). Del-1 bound to the apoptotic cells by recognizing phosphatidyl- serine via the factor VIII-homologous domains with an affinity similar to that of MFG-E8. The phagocytic activity of NIH 3T3 cells against apoptotic cells was enhanced by Del-1 through an interaction between the epidermal growth factor domain in Del-1 and Downloaded from ␣ ␤ v 3 integrin expressed in the NIH 3T3 cells. Screening of primary macrophages and macrophage cell lines for the expression of MFG-E8 and Del-1 indicated that MFG-E8 and Del-1 are expressed in different sets of macrophages. These results suggest the existence of macrophage subsets that use MFG-E8 or Del-1 differently to engulf apoptotic cells. The Journal of Immunology, 2004, 172: 3876–3882. poptosis removes toxic or useless cells in metazoans (1, cells is devoid of phosphatidylserine (14). When apoptosis is in- http://www.jimmunol.org/ 2). It is involved in organ development, tissue remodel- duced in cells, phosphatidylserine is translocated from the inner A ing, and tissue turn over. Apoptosis is induced by intrin- leaflet to the outer leaflet of the plasma membranes (12, 15). This sic and extrinsic stimuli (3, 4) and is mediated by a family of exposure of phosphatidylserine is thought to be mediated by the caspases that cleave a set of cellular substrates and by a specific concomitant activation of the plasma membrane phospholipid DNase (caspase-activated DNase) that degrades the chromosomal scramblase and inhibition of an ATP-dependent aminophospho- DNA (5–7). lipid translocase (16, 17). A number of macrophage receptors have Apoptotic cells are swiftly removed by professional phagocytes been suggested to recognize apoptotic cells, and several of these (macrophages and immature dendritic cells) or amateur phago- molecules including CD36, CD68, and class B scavenger receptor by guest on September 29, 2021 cytes such as fibroblasts and epithelial cells (8, 9). The engulfment type I, were reported to directly bind phosphatidylserine (18–20). of apoptotic cells is believed to benefit animals by preventing the By screening a library of mAbs against the cell surface proteins inflammation and tissue damage that can be caused by intracellular of mouse macrophages, we recently identified a factor that can link materials being released from dying cells. Thus, unless the burden apoptotic cells to macrophages (21). The factor, called milk fat of apoptotic cells exceeds the capacity of the macrophages, most of 3 the apoptotic cells generated during animal development or tissue globule epidermal growth factor-8 (MFG-E8) in mice and lactad- turnover are engulfed by macrophages (10). herin in humans, is comprised of two epidermal growth factor Macrophages engulf apoptotic cells but not living cells, indicat- (EGF) domains and two factor VIII-homologous domains (discoi- ing that apoptotic cells present an “eat me” signal(s) that can be din domain), and is expressed in thioglycolate-elicited peritoneal recognized by macrophages (11). Among various molecules pro- macrophages. In this report, we found that Del-1, originally iden- posed as an “eat me” signal, phosphatidylserine is the most likely tified as a matrix protein expressed in the endothelial cells of candidate (12, 13). Except for myoblasts, which are fusion-com- mouse embryos (22), is highly homologous to MFG-E8 in its petent, the extracellular leaflet of the plasma membrane of living structure and function. The recombinant Del-1 specifically bound to phosphatidylserine through its factor VIII-homologous do- mains, and to ␣ ␤ integrins via an Arg-Gly-Asp motif in the *Department of Genetics, Osaka University Medical School, Osaka, Japan; †Labo- v 3 ratory for Innate Cellular Immunity, RIKEN Research Center for Allergy and Immu- second EGF domain. Del-1 was as potent as MFG-E8 in enhancing nology, Yokohama, Kanagawa, Japan; ‡Core Research for Evolutional Science and the engulfment of apoptotic cells by NIH 3T3 cells. Del-1 was Technology, Japan Science and Technology Corporation, Osaka, Japan; and §Labo- ratory of Genetics, Integrated Biology Laboratories, Graduate School of Frontier Bio- expressed in macrophages, but the type of macrophages expressing sciences, Osaka University, Osaka, Japan Del-1 was different from that expressing MFG-E8. That is, thio- Received for publication September 9, 2003. Accepted for publication January glycolate-elicited macrophages expressed MFG-E8, but not Del-1. 15, 2004. Fetal liver and thymic macrophages expressed Del-1 but not MFG- The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance E8. These results suggested that different macrophages use with 18 U.S.C. Section 1734 solely to indicate this fact. MFG-E8 or Del-1 to engulf apoptotic cells. 1 This work was supported in part by grants-in-aid from the Ministry of Education, Science, Sports, and Culture in Japan. R.H. is supported by a research fellowship from the Japan Society for the Promotion of Science, and M.T. is a recipient of the research grant from the Uehara Foundation. 2 Address correspondence and reprint requests to Dr. Shigekazu Nagata, Department 3 Abbreviations used in this paper: MFG-E8, milk fat globule epidermal growth factor of Genetics, Osaka University Medical School, B-3, 2-2 Yamada-oka, Suita, Osaka 8; EGF, epidermal growth factor; Del-1, developmental endothelial locus-1; wt, wild 565-0871, Japan. E-mail address: [email protected] type, MFG-E8L, MFG-E8 long; MFG-E8S, MFG-E8 short. Copyright © 2004 by The American Association of Immunologists, Inc. 0022-1767/04/$02.00 The Journal of Immunology 3877 Materials and Methods Immunoprecipitation and Western blotting Mice, Armenian hamsters, and cell lines Macrophages (1 ϫ 107 cells) from various sources were cultured in AIM V medium (Invitrogen, Carlsbad, CA) for 48 h. The culture medium was The transgenic mice (ICAD-Sdm) expressing a caspase-resistant form of collected, and adjusted to 1% Triton X-100 as described (28). Del-1 was inhibitor of caspase-activated DNase-short form were described previously then immunoprecipitated with 10 ␮l of anti-Del-1 mAb (clone 4-9)-protein (23). C57BL/6 mice and Armenian hamsters were purchased from Japan A-Sepharose, and eluted from the beads with 30 ␮l of triethylamine (pH SLC (Shizuoka, Japan) and Oriental Yeast (Tokyo, Japan), respectively. 11.7) containing 0.1% Triton X-100. An aliquot (20 ␮l) of the eluate was Macrophages were prepared from the thymus and liver of mouse embryos mixed 1:1 with 2ϫ sample buffer without a reducing agent, separated by as described previously (24). Bone marrow-derived macrophages were ob- 10% PAGE, and the proteins were transferred to a nitrocellulose filter. The tained by culturing bone marrow cells for 7 days in the presence of M-CSF. ␣ ␤ filter was subjected to Western blotting with biotinylated anti-Del-1 mAb Mouse NIH 3T3 transformants expressing integrin v 3 were described previously (21). The NIH 3T3 cells were further transformed with DNase (clone 8-29) and peroxidase-conjugated streptavidin (Roche, Indianapolis, II to enhance the TUNEL reactivity. IN). Proteins recognized by the Ab were visualized using a chemilumines- cence reaction (Western Lightning Chemiluminesence Reagent; Production of rDel-1 and rMFG-E8 PerkinElmer, Wellesley, MA). A DNA fragment for the full-length coding sequence of mouse Del-1 was Protein lipid overlay assay and solid-phase ELISA prepared by RT-PCR with RNA from E15.5 mouse embryo using primers L-␣-phosphatidyl-L-serine, L-␣-phosphatidylcholine, L-␣-phosphatidyleth- whose sequences have been published (22). After joining a FLAG epitope anolamine, and L-␣-phosphatidylinositol were purchased from Sigma- Ј at the 3 end, the Del-1 cDNA was inserted into the pEF-BOS-EX vector Aldrich.
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