| Project/Area Number |
17591041
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | National Hospital Organization Osaka Minami Medical Center Department of Clinical Research |
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Principal Investigator |
OHSHIMA Shiro National Hospital Organization Osaka Minami Medical Center, Department of Clinical Research, The head of Autoimmune disease lab, 臨床研究部・免疫異常疾患研究室長 (50362728)
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| Co-Investigator(Kenkyū-buntansha) |
SAEKI Yukihiko National Hospital Organization Osaka Minami Medical Center, Department of Clinical Research, Director, 臨床研究部, 部長 (40240840)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | retroelement / galectin3 |
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| Research Abstract |
We analyzed the expression of all known retroelements using DNA chip developed by Dr.W Seifarth. We found some expression patterns of retroelements, as shown below.
1)Some Retroelements including HERV-K mRNA are expressed even in normal samples.
Ubiquitous expression
HML-4 (HERV-K) Seq10、K-T47D
HERV-ERI E(4-1)
ERV-9 ERV-9
2)There are no RA-specific expression of Retroelements
3)There are cell-type specific expression patterns for some HERVs (ST, SF and MNC).
ST-specific expression
HML-6 (HERV-K) Seq56
HML-10 (HERV-K (C4)) K-C4
Mammalian ERV MoMLV、OvEV-2
HERV-W
MNC-specific expression
HML-2 (HERV-K) K10、U87Zir
HML-3 (HERV-K) SLE666、Seq34、Seq42
HML-3 (HERV-K) Seq43
HERV-L Seq39、Seq40、Seq45、Seq48、Seq51、Seq58
4)The expressions of some retroelements were reduced in RA synovial tissues.
HML-6 (HERV-K) HML-6、Seq38
HML-3 (HERV-K) RT244、Seq26
HML-nd K (U39937)
ERV-FRD ERV-FRD、Seq46
ERV-9 Seq63、Seq59
The investigation of downstream of L1 retrotransposon showed Galectin3 (Gal-3) and Galectin binding protein (Gal-3 BP) were enhanced in local rheumatoid synovium. Moreover, Gal-3 can induce MMP-1,-3 productions in dose dependent manner. Gal-3 plays the important role in induction of MMPs through IL-1β and TNFα independent pathway. Taken together, Gal-3 might contribute to the bone/cartilage destruction by induction of MMPs in RA.
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