Ca^<2+> signaling induced in tumuor cells by platelets
| Project/Area Number |
09470530
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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 |
Laboratory medicine
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| Research Institution | Ehime College of Health Science |
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Principal Investigator |
OKADA Mariko Ehime College of Health Science, Dept.of Clinical Laboratory Technology, Associate Professor, 臨床検査学科, 助教授 (60111118)
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| Co-Investigator(Kenkyū-buntansha) |
HITSUMOTO Yasuo Ehime University School of Medicine, Dept.of Clinical Laboratory Medicine, Assis, 医学部・付属病院, 助手 (90136333)
TOMINAGA Akio Dept.of Clinical Laboratory Technology, Associate Professor, 臨床検査学科, 助手 (90036450)
SAGAWA Terutaka Dept.of Clinical Laboratory Technology, Assistant Professor, 臨床検査学科, 助手 (90162320)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥11,500,000 (Direct Cost: ¥11,500,000)
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| Keywords | platelet-mediated tumour cell killing / Ca^<2+> signaling / cytosolic Ca^<2+> concentration / thapsigargin / Ca^<2+> stores / ACAS laser cytometry / flow cytometry / 血小板 / 細胞傷害反応 / Fluo-3 / Calcium Green / Fura Red / 細胞内Ca^<2+> / レーザーサイトメーター / flow cytometer / propidium iodide |
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| Research Abstract |
In ordetr to know whether the platelet-mediated killing of tumour cells is regulated by Ca^<2+>, we have investigated early changes in cytosolic Ca^<+2> concentration ([Ca^<2+>]i) in target tumour cells induced by platelets using both ACAS laser cytometry and flow cytometry. K562 and LU99A cells, both of which are sensitive to the cytotoxicity of platelets, and Molt4 cells, which are insensitive to that, were used as target cells. Platelets stimulated not only K562 and LU99A cells but also Molt4 cells to release Ca^<2+> from intracellular stores resulting in transient elevation of [Ca^<2+>]i in those cells. The supematant obtained from thrombin-activated platelets, which has no cytotoxic activity, also induced the rises of [Ca^<2+>]i in K562 cells. These results indicate that the change of [Ca^<2+>]i in target cells in the early phase of the reaction is not the suffucient condition for target cells to be killed by plateles. When Ca^<2+> stores in endoplasmic reticulum of target cells were depleted by thapsigargin, LU99A cells became insensitive to the platelet cytotoxicity, whereas, Molt4 cells became sensitive to that. The sensitivity of K562 cells to the cytotoxicity was not influenced by thapsigargin. These results suggest that Ca^<2+>-dependent pathways are involved in the palatelet-mediated killing of LU99A and Molt4 cells, but that K562 cells are killed by platelets through a Ca^<2+>-independent pathway.
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Report
(3 results)
Research Products
(4 results)
