1991 Fiscal Year Final Research Report Summary
Roll of cellular Signalling systems on intraocular pressure regulation mechanisms.
| Project/Area Number |
02670788
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Ophthalmology
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| Research Institution | Hiroshima University |
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Principal Investigator |
MISHIMA Hiromu Hiroshima Univ. School of Medicine associate Prof., 医学部, 助教授 (20034100)
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| Co-Investigator(Kenkyū-buntansha) |
HIROTA Atsushi Hiroshima Univ. School of medicine Research Associate, 医学部, 助手
FURUMOTO Atsuhito Hiroshima Univ. medical Hospital Research Associate, 医学部附属病院, 助手 (80238691)
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| Project Period (FY) |
1990 – 1991
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| Keywords | Adenosine 3' : 5'-cyclic monophosphate (cAMP) / Protein kinase C (PKC) / Inositol phospholipid turnover system / Cross-talk between cellular signalling systems / Cultured ciliary epithelia (CE) |
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| Research Abstract |
We studied how drugs that alter the inositol phospholopid turnover system affected the adenosine 3' : 5'-cyclic monophosphate(cAMP)system in ciliary epithelial cells to clarify a cross-talk between cAMP system and inositol phospholipid turnover system.
The cAMP increases were observed in cultured chick embryo ciliary epithelial cells stimulated with isoproterenol, forskolin or NaF. The cultured cells pretreated with 2OOnM phorbol 12myristate 13-acetate(PMA), a protein kinase C(PKC)activator showed 42% inhibition of the cAMP increase induced by isoproterenol. When cultured cells incubated with 5OuM H-7, a PKC inhibitor were pretreated with 2OOnti PMA and stimulated with isoproterenol, the inhibitory effect on cAMP increase was reduced.
The cultured cells pretreated with 2OOnM PMA showed 12% inhibition of the cAMP increase induced by forskolin. No inhibition of the cAMP increase was noted in the cultured cells stimulated with NaF after 2OOnM PMA pretreatment.
These findings suggest that inhibition of the cAMP system is caused by the activation of PKC. -adrenergic receptor was regarded as the affected point of PKC.
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