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Clearance of apoptotic cells is not impaired in mouse embryos deficient in class A scavenger receptor types I and II (CD204)
Author(s) -
Komohara Yoshihiro,
Terasaki Yasuhiro,
Kaikita Koichi,
Suzuki Hiroshi,
Kodama Tatsuhiko,
Takeya Motohiro
Publication year - 2005
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20206
Subject(s) - biology , scavenger receptor , microbiology and biotechnology , embryonic stem cell , morphogenesis , cd36 , apoptosis , receptor , endocrinology , biochemistry , lipoprotein , cholesterol , gene
Elimination of apoptotic cells is an important mechanism to maintain proper embryonal morphogenesis. The class A scavenger receptor type I, II (CD204), one of the major receptors expressed on macrophages, is a receptor actively involved in recognition and ingestion of apoptotic cells. To clarify the role of CD204 in embryonic morphogenesis, we performed immunohistochemical and immunoelectron microscopic studies using CD204‐deficient mouse embryos. In control mice, almost all macrophages expressed CD204 from embryonic day 9.5 (E9.5). Phagocytes engulfing dead cells in the E13.5 interdigit region showed strong expression of CD204, indicating that CD204 was actively involved in apoptotic cell clearance. However, CD204 is not essential for the embryonic clearance of apoptotic cells, because CD204‐deficient embryos developed normally without any retardation in footplate remodeling. Up‐regulation of CD36 in CD204‐deficient fetal macrophages suggested that CD36 substitutes for CD204 function. We also found that mesenchymal cells frequently engulfed apoptotic cells especially in early embryonal stages. These data suggest that CD204 is partially but not essentially involved in apoptotic cell clearance in embryogenesis. During early embryonal development, mesenchymal cells, rather than macrophages, play a major role in apoptotic cell clearance. Developmental Dynamics 232:64–74, 2005. © 2004 Wiley‐Liss, Inc.