Morphological and functional analysis of protease-activated receptor 2 on intracellular calcium dynamics in rat parotid gland acinar cells
蛋白酶激活受体2对大鼠腮腺腺泡细胞内钙动态的形态和功能分析
基本信息
- 批准号:21590200
- 负责人:
- 金额:$ 3万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2009
- 资助国家:日本
- 起止时间:2009 至 2011
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Protease-activated receptors(PARs) represent a novel class seven transmembrane domain G-protein coupled receptors, which are activated by proteolytic cleavage. Recent studies have reported that PARs are present in a variety of cells and have been prominently implicated in the regulation of a number of vital functions. The issue of whether the stimulation of PARs induces responses in parotid glands was examined ; with special reference to intracellular Ca^<2+>([Ca^<2+>]_i) dynamics during PARs stimulation. In the present study, PAR2 mRNA was expressed strongly in the parotid glands. In parotid acinar cells, PAR2-activating peptide(PAR2-AP), SLIGRL-NH_2, induced an increase in[Ca^<2+>]_i. Both removing of extracellular Ca^<2+> and using of Ca^<2+> channel blockers did not inhibit the PAR2-AP-induced[Ca^<2+>]_i increase. The response to PAR-2 activation was mainly caused by Ca^<2+> mobilization from intracellular Ca^<2+> stores. This peptide induced Ca^<2+> release and entry were partially inhibited by the nitric oxide synthase(NOS) inhibitor, L-NAME. The NO donor, GEA 3162, but not 8-bromo-cGMP, mimicked the effects of PAR2 in activating non capacitative calcium entry(NCCE). Both KN93(a CAM kinase II inhibitor) and W7(a calmodulin inhibitor) completely blocked a Ca^<2+> release from intracellular Ca2+store and a Ca^<2+> influx from extracellular spaces. Tetracaine and DHAB partially blocked these increases. These results indicate that PAR2-AP activates NCCE pathway. And we proposed that an effect of PAR-2 in parotid gland is dependent on CAMKII and a PAR2-AP activates the ryanodine-like receptors.
蛋白酶激活受体(PARs)是一类新型的跨膜结构域G蛋白偶联受体,通过蛋白水解作用被激活。最近的研究报道,PAR存在于各种细胞中,并且显著地涉及许多重要功能的调节。研究了刺激PAR是否诱导腮腺反应的问题;特别是在PAR刺激期间细胞内Ca^<2+>([Ca^<2+>]_i)动态。在本研究中,PAR 2 mRNA在腮腺中强烈表达。在腮腺腺泡细胞中,PAR 2激活肽(PAR 2-AP)SLIGRL-NH_2可诱导[Ca^<2+>]_i增加。去除细胞外Ca^<2+>和使用Ca^<2+>通道阻断剂均不能抑制PAR 2-AP诱导的[Ca^<2+>]_i升高。对PAR-2激活的反应主要是由细胞内Ca^2+库的Ca^2+动员引起的。该肽诱导的Ca^2+释放和内流可被一氧化氮合酶(NOS)抑制剂L-NAME部分抑制。NO供体GEA 3162(而不是8-溴-cGMP)模拟了PAR 2激活非容量性钙内流(NCCE)的作用。KN 93(一种CAM激酶II抑制剂)和W7(一种钙调蛋白抑制剂)都能完全阻断细胞内Ca ^2+库的Ca^2+释放和细胞外Ca ^2+内流。丁卡因和DHAB部分阻断了这些增加。这些结果表明PAR 2-AP激活NCCE通路。我们认为PAR-2在腮腺中的作用依赖于CAMK Ⅱ,PAR-2-AP激活ryanodine样受体。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
New era of morphology-Developed by the fluorescent markers and the confocal microscopy.
形态学的新时代-由荧光标记和共焦显微镜开发。
- DOI:
- 发表时间:2010
- 期刊:
- 影响因子:0
- 作者:Satoh Y;Saino T;Akutsu-Yamauchi H;Hamano Y
- 通讯作者:Hamano Y
細胞内カルシウム動態を指標としたラット耳下腺におけるProtease-activated receptor 2の機能解析
以细胞内钙动态为指标的大鼠腮腺蛋白酶激活受体2功能分析
- DOI:
- 发表时间:2009
- 期刊:
- 影响因子:0
- 作者:齋野朝幸;ワトソンアイリーン;佐藤洋一
- 通讯作者:佐藤洋一
CalmodulinあるいはCalmodulin kinase IIの抑制によってラット耳下腺におけるProtease activated receptor 2誘発性のCa^<2+>上昇が完全抑制される
钙调蛋白或钙调蛋白激酶II的抑制完全抑制大鼠腮腺中蛋白酶激活受体2诱导的Ca 2+ 升高。
- DOI:
- 发表时间:2009
- 期刊:
- 影响因子:0
- 作者:齋野朝幸、Eileen L. Watson;佐藤洋一
- 通讯作者:佐藤洋一
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SAINO Tomoyuki其他文献
SAINO Tomoyuki的其他文献
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{{ truncateString('SAINO Tomoyuki', 18)}}的其他基金
Morphological and functional analysis which protein phosphatasesplay a role in regulating the exocrine mechanism
蛋白磷酸酶对外分泌调节机制的形态和功能分析
- 批准号:
18590192 - 财政年份:2006
- 资助金额:
$ 3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)