| Co-Investigator(Kenkyū-buntansha) |
CHIKAMA Tai-ichiro Yamaguchi University, Hospital, Lecturer, 医学部・附属病院, 講師 (00263765)
KUMAGAI Naoki Yamaguchi University, School of Medicine, Assistant professor, 医学部, 助教授 (20234510)
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| Budget Amount *help |
¥14,900,000 (Direct Cost: ¥14,900,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2000: ¥12,700,000 (Direct Cost: ¥12,700,000)
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| Research Abstract |
In a clinical setting, the corneal epithelial defects often persisted in those who lost corneal sensation. Furthermore, the persistence of epithelial defects leads to the corneal ulcer, that is the excess collagen degradation. We have reported that sensory neurotransmitter, substance P stimulates corneal epithelial migration in the presence of IGF-1. In this research projects, we found the followings. 1) The synergistic effects of substance P and IGF-1 require the participation of protein kinase C, tyrosine kinase, phosphoinositol 3-kinase and p38 mitogen-activated protein kinase. 2) Small GTP-binding protein, Rho, participated in the stimulation of corneal epithelial migration. 3) Laminin, one of the basement membrane proteins, regulates the expression of junctional proteins, which locate at the adhesion apparatus between the corneal epithelial cells during wound healing. 4) Corneal fibroblasts and PMN synergistically stimulate the collagen degradation through IL-1 system. 5) Cytokines, TNF-a and IL-13 stimulates production of chemokine, eotaxin, in corneal fibroblasts. 6) The stimulation of corneal epithelial cells by substance P and IGF-1 changes the expression profiles of various mRNAs.
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