1993 Fiscal Year Final Research Report Summary
The transmembrane mechanism on neuroimmune interaction
| Project/Area Number |
04454528
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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 |
Biological pharmacy
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| Research Institution | Hokkaido University |
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Principal Investigator |
YASUYUKI Nomura Hokkaido Univ..Fac.Pharm.. Prof., 薬学部, 教授 (00034041)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Neuroimmune interaction / Human lymphocyte / Cytokine / Interleukin 2 / NG 108-15 cell / Neurite elongation / Glial cell / Nitric acid dynthase |
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| Research Abstract |
To clarigy functional significances and the transmenbrane signgalling mechanism of neurotransmitter actions in lymphocytes and cytokine actions in neurons, we inverstigated cellular responses, in particular gene expression of physiological active molecules, to acetylcholine in T cells and to LPS in glial cells and to NO in neurons.
We found that : 1) m_3 type of acetylcholine receptors is present in human T cells and the stimulation causes inositol 3-phosphate fromation followed by an increase in [Ca^<2+>]i, 2)m_3 receptors seem to be involved in potentiation of lectin-induced formation of IL-2 and IL-2 receptors.
We also obtained interesting findings that : 1) LPS induces de novo sythesis of nitric oxide synthase (iNOS) in glial cells via 110 kDa proteins phosphorylated by protein tyrosine kinase, 2) NO generated by iNOS in glial cells probably penetrates into surrounding neurons an causes cell death.
We succeeded cloning and sequencing of cDNA of a novel neuronal differentiation factor, TA 20 from NG108-15 cells and found that TA 20 is a protein with molecular size of approx. 20 kDa whose gene expression is activated by treatment with TPA and dibutylyl cAMP.We are further examining functional roles of TA20 and mechanism of the gene espression.
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