1998 Fiscal Year Final Research Report Summary
Establishment of experimental model by using gene transfer and Leukemia Inhibitory Factor (LIF) "knock-out" mouse
| Project/Area Number |
09671502
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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 |
Orthopaedic surgery
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| Research Institution | Nagasaki University |
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Principal Investigator |
FUJII Tohru Nagasaki University School of Medicine Professor, 医学部, 教授 (60136661)
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| Co-Investigator(Kenkyū-buntansha) |
AKITA Sadanori Nagasaki University School of Medicine Hospital Staff Physician, 医学部附属病院, 医員
YAMANOBE Yuuji Nagasaki University School of Medicine Hospital Assistant, 医学部附属病院, 助手 (40284690)
HIRANO Akiyoshi Nagasaki University School of Medicine Assistant Professor, 医学部, 助教授 (90208835)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Leukemia Inhibitory Factor (LIF) / Wound healing / immunity in grafting / signal transduction |
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| Research Abstract |
The pituitary specific leukemia inhibitory factor (LIF) transgenic mouse revealed the significant morphological and molecular changes, which is expressed by the systemic dwarfism and the hormone producing cells in pituitary altered.
The growth hormone secreting cell implantation in the adult rats resulted in the positive correlation between mandibular bone augmentation and strong LIF expression shown by in situ hybridyzation.
The keloid-devived fibroblast cell culture study showed the IGF-1 receptor was specifically expressed among the tyrosine-type receptor subtypes and IGF-l was able to regulate the invasiveness of the keloid-derived fibroblast cells.
This may explain that the IGF-l and its receptor pathway markedly related to the keloid mechanism and signal transduction.
[IF is highly expressed in patients with psoriasis and contact dermatitis and its over-expression in local skin tissue could prolong the allogeneic skin grafting at 12, 24 and 72 hours after skin grafting on mouse back l.5x1.5 cm in between B6D2F1 and BALB/c strains. LIF Over-expressed allogeneic skin grafting resulted in the immune tolerance. This immune tolerance was regulated by LIF expressiona and and expressions of subsequent proper LIF receptor and signal transducing component namely gpl3O.Classical helper T cell expression such as Thl by IL-2 and Th2 by IL-10 were not detected. Thus this phenomena may be LIF specific and LlF may be most important regulator for the prolonged.
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