2005 Fiscal Year Final Research Report Summary
Research for the role of stress protein in TMD
| Project/Area Number |
16591992
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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 |
Surgical dentistry
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| Research Institution | Osaka University (2005)
Kyoto University (2004) |
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Principal Investigator |
YAMAMURA Isao Osaka university, Faculty of dentistry, Assistant Professor, 大学院歯学研究科, 助手 (90332733)
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| Co-Investigator(Kenkyū-buntansha) |
NAGATA Kazuhiro Kyoto University, Institute for Frontier medical Science, Professor, 再生医学研究所, 教授 (50127114)
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| Project Period (FY) |
2004 – 2005
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| Keywords | TMD / stress protein |
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| Research Abstract |
I confirmed HSP27, HSP70 and expression of HSP90 by RT-PCR method in the cultured synovial cells derived from the patients of temporomandibular arthrosis or TMJ synovialosteochondromatosis. And these results might be considered that these cells expressed the HSPs to be coped with stress of the outside. And I confirmed, Sex hormones, estrogen receptors ER-α and ER-β were expressed in these cells by RT-PCR method. HSP27 is suggesuted that it participates in the estrogen signal transduction. I confirmed induction of the expression of HSP27 gene by RT-PCR method in dose-dependent manner of β-estradiol when I examined influence to give to expression of HSP27 by estrogen, but the difference that was clear by Northen-Blot method was not recognized. To
Investigate this difference, I construct the plasmids consist of 5' promoter region of human HSP27 gene fused to a firefly luciferase gene, as a reporter gene, and analyzed the activatin of promoter activity of HSP27 gene by β-estradiol stimulation in the human synonvial cells. As the results, the increase of transcriptional activity by β-estradiol was confirmed in some cell lines, but was not in all cell lines. As this cause, the possibility that the mechanism of the transcriptional activation of HSP27 gene by β-estradiol having falls off it is originally thought about in each cell strain and is going to investigate a cause of the difference in future.
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[Journal Article] Advanced glycation end products increase collagen-specific chaperone protein in mouse diabetic nephropathy.2004
Author(s)
OHASHI, H.ABE, T.TAKAHASHI, Y.YAMAMOTO, M.TAKEUCHI, H.ARAI, K.NAGATA, T.KITA, H.OKAMOTO, H.YAMAMOTO, T.DOI.
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Journal Title
J.Biol.Chem. 279(19)
Pages: 19816-19823
Description
「研究成果報告書概要(欧文)」より
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