Project/Area Number |
21590435
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Nagoya University |
Principal Investigator |
MURAKUMO Yoshiki 名古屋大学, 大学院・医学系研究科, 准教授 (40324438)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 疾患モデル動物 / CD109 / ノックアウトマウス / 表皮ケラチノサイト / 初代培養 / STAT3 / TGFβ / トランスジェニックマウス / 結合蛋白 / 体毛発育異常 / 表皮過形成 / TGFssシグナル / 免疫組織化学染色 / 脱毛 / 精子形成 |
Research Abstract |
We generated CD109 knockout mouse to assess biological significance of GPI-anchored protein CD109 in mouse development. In wild-type mouse, CD109 expression was detected in basal and suprabasal region of the epidermis and seminiferous tubules of the testis. CD109./. mice could be alive and showed transient hair-loss from postnatal day 7(P7) to P28. CD109./. male and female mice were fertile. Histopathological analyses revealed that epidermal hyperplasia was detected in CD109./. mice from P7 to P70, and ectatic hair follicles were apparent from p14 to p21. Since epidermal hyperplasia was seen in dorsal skin epidermis, which does not have hair and hair follicles, we thought that CD109-deficiency develops epidermal hyperplasia, which leads to ectatic hair follicle and hair-loss. Immunohistochemical analyses revealed that STAT3 phosphorylation was apparently upregulated compaired with wild-type mice, suggesting that STAT3 signaling may be associated with epidermal hyperplasia of CD109./. mice. Next, we tried to detect secreted CD109 and to identify its interaction partners in the serum of CD109 transgenic mice. Secreted CD109 in mouse serum was detected by Western blotting, however, we could not identify candidates of CD109-interaction proteins in this experiment. Then, we attempted to identify CD109-interaction proteins in the medium of CD109-overexpressing culture cells. We successfully identified a candidate of CD109-interaction protein in this experiment, and now we are investigating biological significance of the interaction between CD109 and the interaction protein.
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