2013 Fiscal Year Final Research Report
Analysis of Dock8 and ASK1 functions in optic nerve regeneration
| Project/Area Number |
24791884
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
KITTAKA Daiji 公益財団法人東京都医学総合研究所, 運動・感覚システム研究分野, 研究員 (50623782)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | ASK1 / 視神経再生 / 炎症 |
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| Research Abstract |
Neurons are normally unable to regenerate their axons in the central nervous system, but neuroinflammation induced by a proinflammatory agent such as zymosan stimulates axonal regeneration. Apoptosis signal-regulating kinase 1 (ASK1) is an evolutionarily conserved mitogen-activated protein kinase kinase kinase (MAP3K) and plays important roles in neural cell death and inflammation. In the present study, we found that zymosan-stimulated optic nerve regeneration is severely suppressed in ASK1-deficient mice. ASK1 was required for the zymosan-stimulated migration of macrophages into the mouse retina, and oncomodulin production in macrophages and retinal Müller glia. However, ASK1 deficiency in retinal ganglion cells had no effect on axonal outgrowth. These results suggest that ASK1 signaling in non-neuronal cells plays important roles in zymosan-stimulated optic nerve regeneration.
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[Journal Article] Inhibition of ASK1-p38 pathway prevents neural cell death following optic nerve injury2013
Author(s)
Katome, T., Namekata, K., Guo, X., Semba, K., Kittaka, D., Kawamura, K., Kimura, A., Harada, C., Ichijo, H., Mitamura, Y. and Harada, T
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Journal Title
Cell Death and Differentiation
Volume: 20
Pages: 270-280
Peer Reviewed
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