1993 Fiscal Year Final Research Report Summary
Fundamental research for the complex lipid change during wound healing
| Project/Area Number |
04454309
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | University of Tokyo |
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Principal Investigator |
HARII Kiyonori University of Tokyo Medical Department Professor, 医学部(病), 教授 (50111539)
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| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Yasushi University of Tokyo Medical Department Staff, 医学部(病), 医員
YOSHIMURA Koutaro University of Tokyo Medical Department Staff, 医学部(病), 助手 (60210762)
KAWASHOMA Takao University of Tokyo Medical Department Staff, 医学部(病), 助手 (20214637)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Wound healing / Epidermal lipid / Cholesterol sulfate / Cholesterol ester |
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| Research Abstract |
Little is known about changes in the lipid composition of the skin during fetal development and wound healing. In these studies, we investigated the lipid composition of human fetal epidermmis ranging from 14 week to 28 week estimated gestational ages epidermis(EGA) and fetal mouse epidermis ranging 14 day EGA to delibvery. The lipid composition of epidermal fractions from human skin samples between 14w to 17w EGA was exhibiting a predominance of free sterols, free fatty acid, phospholipids and squalene. After 20 w EGA fetal epidermis became enriched in cholesterol derivatives, ceramids and glycosylceramids. Moreover cholesterol ester became prominent comparing with newborn and adult epidermis. In mouse epidermis, along with the formation of the multilayred structure of the epidermis, cholesterol sulfate concentration of cholesterol sulfate increased. Cholesterol sulfotransferase showed a 6-fold increase from 14 to day 16 EAG with appearance of cholesterol sulfate.
Abnormal wound healing process causes keloid, exhibiting hyperproliferation of extracellular matrix. Keloid was obtained surgically, and the epidermal thickness of keloid was measured and compared the normal looking skin of the same patient. Keloidal epidermis showed marked thickness but the proportion of the four epidermal layrs was not changed. The lipid composition of keloid epidermis was determined and compared with normal looking skin around the lesion. There was a significant decrease in squalene and triglyceride contents compared with the normal epidermis. Squalene and triglyceride are major components of sebaceous gland lipids. Lack of them may make epidermis dry, which in turn causes barrier dysfunction. Recently barrier abnormality results in epidermal hyperproliferation, scaling and inflammation. The lack of sebaceous lipids in keloid may cause the hyperproliferation of epidermis. Keloid may serve a unique model to clarify the role of sebaceous lipids in the whole epidermal lipid function.
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