1997 Fiscal Year Final Research Report Summary
Immunocytochemical study on the mechanisms of phagocytotic elimination of apoptotic ameloblasts in rat incisors
| Project/Area Number |
08672107
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
NISHIKAWA Sumio Tsurumi University School of Dental Medicine, Derpartment of Biology, Lecturer, 歯学部, 講師 (60097277)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Ameloblasts / Apoptosis / Phagocytosis / Immunohistochemistry / Cell nucleus |
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| Research Abstract |
The head investigator of this research project has previously reported on the apoptosis of ameloblasts in rat incisors. Based on results that showed that ameloblasts in the transitional zone between secretion and maturation die in part via apoptosis, it is shown in this study that fragmented apoptotic ameloblasts are eliminated by the phagocytotic activity of neighboring ameloblasts, epithelial cells in the papillary layr, and macrophage-like cells. The macrophage-like cells invade the papillary layr in the transitional zone, and express MHC class II antigen at their plasma membrane. Thus, it is possible that the macrophages ingesting apoptotic cell fragments present self-antigens derived from phagocytosed ameloblasts. Throughout apoptosis, the relocation or disappearance of U class snRNA serving pre-mRNA processing and several RNA-related proteins occurs in the nucleus, in addition to well-known DNA relocation. Ameloblasts are culled by apoptosis in the transition stage, probably because a large number of ameloblasts are no longer necessary to mature enamel matrix. It will be necessary to investigate whether or not apoptosis occurs in diverse tooth-related tissues and what triggers tooth apoptosis
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