2013 Fiscal Year Final Research Report
Development of new drugs based on molecular mechanism for infectious corneal ulcer
| Project/Area Number |
23592572
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SONODA Koh-hei 山口大学, 大学院医学系研究科, 教授 (10294943)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 角膜潰瘍 / 感染 / ｺﾗｰｹﾞﾝ分解 / MMP |
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| Research Abstract |
Collagen degradation of corneal stroma relates to the etiology of corneal ulcerration.Moreover,Corneal fibroblasts contribute to collagen remodeling in the corneal stroma in part by mediating collagen degradation.Corneal structure is influenced by sex hormone status,we examined the effects of sex hormones on collagen degradation by corneal fibroblasts.17beta-Estradiol and progesterone,female sex hormones,inhibited interleukin (IL)-1beta-induced collagen degradation,whereas testosterone and DHEA had no such effect.MMP expression and activation in corneal fibroblasts exposed to IL-1beta were also inhibited by them.They nhibited the IL-1beta-induced phosphorylation of p38 MAPK without affecting that of the MAPKs ERK or JNK.17beta-Estradiol also inhibited the IL-1beta-induced phosphorylation of IkappaB-alpha.Female sex hormones inhibited MMP expression and activity in IL-1beta-stimulated corneal fibroblasts and thereby suppressed collagen degradation by these cells.
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