Expression of collagenase and collagenase inhibitors mRNA in periodontitisaffected human gingival tissue.
Project/Area Number |
03454440
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Research Category |
Grant-in-Aid for General Scientific Research (B)
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Allocation Type | Single-year Grants |
Research Field |
Conservative dentistry
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Research Institution | Niigata University |
Principal Investigator |
YOSHIE Hiromasa Niigata University, School of Dentistry, Associate Professor, 歯学部, 助教授 (20143787)
|
Co-Investigator(Kenkyū-buntansha) |
OKUDA Kazuhiro Niigata University Dental Hospital, Lecturer, 歯学部・附属病院, 講師 (00169228)
YAMAZAKI Kazuhisa Niigata University Dental Hospital, Lecturer, 歯学部・附属病院, 講師 (00182478)
|
Project Period (FY) |
1991 – 1992
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Project Status |
Completed (Fiscal Year 1992)
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Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1991: ¥5,300,000 (Direct Cost: ¥5,300,000)
|
Keywords | TIMP-gene / Collagenase-gene / Periodontitis / RT-PCR / 逆転写PCR法 / 歯肉 / コラゲナ-ゼ / TIMP |
Research Abstract |
Collagenolysis in periodontitis is thought to be modulated by the expression of three genes, collagenase, tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and-2). We assessed the possible difference in TIMP-1, TIMP-2 and collagenase mRNA levels between gingival samples from patients with periodontitis and those from healthy subjects by reverse transcription-polymerase chain reaction (RT- PCR). This technique allows detection of transcripts from a very small sample quantity. The experiments showed that levels of TIMP-1 and collagenase transcripts relative to beta-actin are significantly higher in the diseased group than in health controls (8.11*0.83 versus 1.38*0.28% for TIMP-1 and 0.50*0.10 versus 0.0075*0.0024% for collagenas, respectively). The difference in TIMP-2 between the two groups(2.91*0.46 versus 1.84*0.87%) did not differ. Therefore, the host would have responded to the increase in collagenase level by preferentially producing TIMP-1 against tissue destruction. The differential gene expression of TIMP-1 and TIMP-2 in our study may account for a distinct genetic regulation of TIMP-1 and -2 in vivo.
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Report
(3 results)
Research Products
(6 results)