1996 Fiscal Year Final Research Report Summary
Apoptosis in nifedipine-induced gingival overgrowth in rats.
| Project/Area Number |
07457457
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Conservative dentistry
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| Research Institution | The University of Tokushima, University of Dental Hospital |
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Principal Investigator |
NISHIKAWA Seiji The University of Tokushima, University of Dental Hospital, Assistant Professor, 歯学部・附属病院, 講師 (80208157)
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| Co-Investigator(Kenkyū-buntansha) |
KIDO Jun-ichi The University of Tokushima, University of Dental Hospital, Assistant Professor, 歯学部・附属病院, 講師 (10195315)
SHINOHARA Hiroyuki The University of Tokushima, The University of Tokushima School of Dentistry, Re, 歯学部, 助手 (60175388)
ISHIDA Hiroshi The University of Tokushima, The University of Tokushima School of Dentistry, As, 歯学部, 助教授 (90127803)
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| Project Period (FY) |
1995 – 1996
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| Keywords | nifedipine / gingival overgrowth / apoptosis |
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| Research Abstract |
Recently, we established an experimental model of gingival overgrowth induced by Ca^<2+> channel blocker, nifedipine in rats. In this study, we examined the relationship between nifedipine-induced gingival overgrowth and apoptosis, which serves to counterbalance mitosis in a cell population. We found that the activity of tissue transglutaminase (TG), one of the few effector elements of apoptosis, in nifedipine-treated rats was lower than that in control rats. The number of apoptotic cells in the gingival tissue, as determined by nick-end labeling and immunohistochemical analysis of proliferatind cell nuclear antigen, was decreased by nifedipine administration. Since some apoptotic-relating enzymes including TG and endonuclease are Ca^<2+>-dependent, blockade of one or more steps in the cascade of apoptosis by nifedipine may result in a change in the apoptosis rate, leading to an increase in the net growth rate of gingival tissue.
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