Project/Area Number |
13680826
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | JIKEI UNIVERSITY SCHOOL OF MEDICINE (2002-2003) Keio University (2001) |
Principal Investigator |
IKESHIMA Hiroko JIKEI UNIVERSITY SCHOOL OF MEDICINE, Research Assistant, 医学部, 助手 (60265783)
|
Project Period (FY) |
2001 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
Keywords | tenascin / knockout mouse / astrocytes / central nervous systems / regeneration / glyosis / lesion / wound-healing / 創傷治癒 |
Research Abstract |
In primary culture of astrocytes there can be classified morphologically into two types : fibrous and protoplasmic astrocytes. In this study we have analyzed for primary astrocytes of in vitro culture compared with those from wild type and tenascin-deficient mouse. We found that the fibrous astrocytes, which are expressing tenascin at high level in primary astrocytes from wild type mouse, were never appeared in those from tenascin-deficient mouse. Furthermore the protoplasmic astrocytes, which are expressing tenascin at low level, also did not appeared with tiled shapes in primary culture of astrocytes from tenascin-deficient. By the cell proliferation assay, we demonstrate that tenascin-expressing astrocytes are involved in cell proliferation in primary culture of astrocytes. These results suggested that tenascin is an essential molecule for maintaining proper cell morphology and function in primary astrocytes. The expression of tenascin, one of the astroglia-derived extracellular matrix proteins, isup-regulated in sites of injured brain of the mouse. In vitro study showed neurite outgrowth was inhibited when neurons were co-cultured with tenascin-expressing astrocytes. In light of these observations it is propagated that tenascin-expressing astrocytes could be involved in the inhibition of CNS regenerationafter brain injury. To investigate the role of tenascin played in the regeneration process of the CNS astrocytes of the tenascin-deficient mouse were studied after a stab wound was made to the brain. The blood-brain barrier permeability in these micewas also analyzed during the wound-healing process.
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