2007 Fiscal Year Final Research Report Summary
Study of function of ADAMTS-1 in skin wound healing
| Project/Area Number |
18590365
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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 |
Experimental pathology
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| Research Institution | Kanazawa University |
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Principal Investigator |
KUNO Kouji Kanazawa University, Cancer Research Institute, Associate Professor (40242565)
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| Project Period (FY) |
2006 – 2007
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| Keywords | ADAMTS / metalloproteinase / 損傷治癒 |
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| Research Abstract |
ADAMTS-1 is a metalloproteinase associated with extracellular matrix that has proteoglycandegrading activity and anti-angiogenic activity. By analyzing ADAMTS-1 gene knockout mice, we have shown that ADAMTS-1 is a multifunctional metalloproteinase that is essential for the structure and function of the ureteropelvic junction as well as ovulation, follicular development, and maintenance of the follicle structure in the ovary. Skin wound healing is a multiple-step process consisting of an inflammation phase, a proliferation phase, and a maturation phase. Since ADAMTS-1 is a gene whose expression is upregulated in the inflammatory condition, in the present study we evaluated whether ADAMTS-1 is involved in the skin wound healing process. Excisonal full-thickness skin wounds were made on the dorsal skin of ADAMTS-1 null mice with a sterile disposable biopsy punch with a diameter 4mm, and changes in wound areas were monitored as an index of wound repair. Three days after injury, wound closure in ADAMTS-1 null mice was delayed compared with that in control mice. Thereafter, the wound area of ADAMTS-1 null mice remained larger than those of control mice until ten days after injury. These observations demonstrated that ADAMTS-1 plays an important role in the skin wound healing process. After we found this phenomenon, another research group reported that ADAMTS-1 regulates the angiogenic response during tissue repair, but further investigation will be necessary to understand the detailed mechanism of delayed wound healing in ADAMTS-1 null mice.
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