| Project/Area Number |
09470006
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
MARUYAMA Yoshio School of Medicine, Tohoku University, 大学院・医学系研究科, 教授 (00133942)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥12,900,000 (Direct Cost: ¥12,900,000)
Fiscal Year 1999: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1997: ¥9,000,000 (Direct Cost: ¥9,000,000)
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| Keywords | endoplasmic reticulum / membrane capacitance / patch-clamp / calcium / vesicle formation / ion channels / pancreatic acinar cells / calcium signaling / Ca_<2+>濃度 / 出芽 / Ca_<2+>シグナル / 粗面小胞体膜 / maxi-Kチャネル / Clチャネル / 肝細胞 / イベリオトキシン / アセチルコリン受容体 / カルシウムシグナル / オルガネラ膜 / 膜容量計測法 / 小胞体Ca / Kチャネル / Ca応答 |
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| Research Abstract |
The present research results could be summarized following 6 subjects as ; 1) Dynamics of vesicle formation controlled by the lumenal CaィイD12+ィエD1 in mammalian endoplasmic reticulum ; We monitored the changes in membrane capacitance (Cm) using a intact lumen ER preparation by varying the lumenal CaィイD12+ィエD1 concentration ([CaィイD12+ィエD1]). A rise and fall in the [CaィイD12+ィエD1] increased and decreased the Cm of the whole-ER membrane, respectively ; 2) A regulatory role of endoplasmic reticulum (ER) ion channels in CaィイD12+ィエD1 release mechanisms of pancreatic acinar cells ; The paper provides a temporal list of ion channels present in the ER. The ER specific channels may influence CaィイD12+ィエD1 signaling ; 3) A putative role of endoplasmic reticulum maxi-K channels in CaィイD12+ィエD1 transport mechanisms between cellular compartments in polarized cells. The paper provide evidence that ER maxi-K channels play a role for a homogenous distribution of CaィイD12+ィエD1 in the storage pools ; 4) Larg
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e conductance anion channels in ER membranes of muse liver cells ; The predominant channel was a large conductance anion selective channel that exhibited voltage dependence and allowed large organic anions to pass ; 5) G protein modulation of voltage-sensitive ACh-binding in muscarinic CaィイD12+ィエD1-signaling of mouse pancreatic acinar cells ; Monitoring the muscarinic CaィイD12+ィエD1-responses, we examined the mechanism of G protein-receptor interaction in terms of the membrane potential. The results indicate that ACh binding is sensitive to the membrane potential and that the G protein association-dissociation cycle modulates the voltage-sensitivity ; 6) Cyclic ADP-ribose elimination from muscarinic CaィイD12+ィエD1-signaling in pancreatic acinar cells studied using CD38 knockout mice. The majority of the cellular cyclic ADP-ribose (cADPR) has been ascribed to the activity of ADP-ribosyl cyclase of CD38. By estimating ACh-induced CaィイD12+ィエD1 responses in pancreatic acinar cells from CD38 knockout mice, we distinguished and characterized individual CaィイD12+ィエD1 pools responsive to cADPR, ryanodine, and IPィイD23ィエD2 by monitoring ACh-evoked increases in the cytosolic CaィイD12+ィエD1 concentration. Less
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