• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

缓激肽介导的 Ca 信号调节人心脏 c-Kit 祖细胞的细胞生长和迁移。

Bradykinin-mediated Ca signalling regulates cell growth and mobility in human cardiac c-Kit progenitor cells.

机构信息

Xiamen Cardiovascular Hospital, Xiamen University, Xiamen, Fujian, China.

Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong Pokfulam, Hong Kong, China.

出版信息

J Cell Mol Med. 2018 Oct;22(10):4688-4699. doi: 10.1111/jcmm.13706. Epub 2018 Aug 17.

DOI:10.1111/jcmm.13706
PMID:30117680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6156395/
Abstract

Our recent study showed that bradykinin increases cell cycling progression and migration of human cardiac c-Kit progenitor cells by activating pAkt and pERK1/2 signals. This study investigated whether bradykinin-mediated Ca signalling participates in regulating cellular functions in cultured human cardiac c-Kit progenitor cells using laser scanning confocal microscopy and biochemical approaches. It was found that bradykinin increased cytosolic free Ca ( ) by triggering a transient Ca release from ER IP3Rs followed by sustained Ca influx through store-operated Ca entry (SOCE) channel. Blockade of B2 receptor with HOE140 or IP3Rs with araguspongin B or silencing IP3R3 with siRNA abolished both Ca release and Ca influx. It is interesting to note that the bradykinin-induced cell cycle progression and migration were not observed in cells with siRNA-silenced IP3R3 or the SOCE component TRPC1, Orai1 or STIM1. Also the bradykinin-induced increase in pAkt and pERK1/2 as well as cyclin D1 was reduced in these cells. These results demonstrate for the first time that bradykinin-mediated increase in free via ER-IP3R3 Ca release followed by Ca influx through SOCE channel plays a crucial role in regulating cell growth and migration via activating pAkt, pERK1/2 and cyclin D1 in human cardiac c-Kit progenitor cells.

摘要

我们最近的研究表明，缓激肽通过激活 pAkt 和 pERK1/2 信号来增加人心肌 c-Kit 祖细胞的细胞周期进展和迁移。本研究采用激光共聚焦显微镜和生化方法研究了缓激肽介导的 Ca 信号是否参与调节培养的人心肌 c-Kit 祖细胞的细胞功能。结果发现，缓激肽通过触发 ER IP3Rs 从细胞内释放瞬时 Ca2+，随后通过储存操作的 Ca2+内流（SOCE）通道持续 Ca2+内流，从而增加细胞浆游离 Ca2+（[Ca2+]i）。用 HOE140 阻断 B2 受体、用 araguspongin B 阻断 IP3Rs 或用 siRNA 沉默 IP3R3，均可消除 Ca2+释放和 Ca2+内流。有趣的是，在沉默 IP3R3 的细胞或缺乏 SOCE 成分 TRPC1、Orai1 或 STIM1 的细胞中，没有观察到缓激肽诱导的细胞周期进展和迁移。此外，在这些细胞中，缓激肽诱导的 pAkt 和 pERK1/2 以及 cyclin D1 的增加也减少了。这些结果首次表明，缓激肽通过 ER-IP3R3 Ca2+释放介导的游离 Ca2+增加，随后通过 SOCE 通道的 Ca2+内流，在调节人心肌 c-Kit 祖细胞的细胞生长和迁移中发挥关键作用，其机制是通过激活 pAkt、pERK1/2 和 cyclin D1。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/e6fed312d263/JCMM-22-4688-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/c3a7ec07becb/JCMM-22-4688-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/9ff0f577c6c8/JCMM-22-4688-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/16c1eadcab17/JCMM-22-4688-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/e8cca765f8d0/JCMM-22-4688-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/91b522818209/JCMM-22-4688-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/19e057bf205c/JCMM-22-4688-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/e6fed312d263/JCMM-22-4688-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/c3a7ec07becb/JCMM-22-4688-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/9ff0f577c6c8/JCMM-22-4688-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/16c1eadcab17/JCMM-22-4688-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/e8cca765f8d0/JCMM-22-4688-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/91b522818209/JCMM-22-4688-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/19e057bf205c/JCMM-22-4688-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/826d/6156395/e6fed312d263/JCMM-22-4688-g007.jpg

相似文献

1
Bradykinin-mediated Ca signalling regulates cell growth and mobility in human cardiac c-Kit progenitor cells.缓激肽介导的 Ca 信号调节人心脏 c-Kit 祖细胞的细胞生长和迁移。
J Cell Mol Med. 2018 Oct;22(10):4688-4699. doi: 10.1111/jcmm.13706. Epub 2018 Aug 17.
2
Roles of store-operated Ca2+ channels in regulating cell cycling and migration of human cardiac c-kit+ progenitor cells.储存式钙通道在调节人类心脏c-kit+祖细胞的细胞周期和迁移中的作用。
Am J Physiol Heart Circ Physiol. 2015 Nov 15;309(10):H1772-81. doi: 10.1152/ajpheart.00260.2015. Epub 2015 Oct 9.
3
Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells.缓激肽调节培养的人心脏c-Kit+祖细胞的细胞生长和迁移。
Oncotarget. 2017 Feb 14;8(7):10822-10835. doi: 10.18632/oncotarget.14609.
4
STIM1 at the plasma membrane as a new target in progressive chronic lymphocytic leukemia.质膜上的 STIM1 作为进展性慢性淋巴细胞白血病的新靶点。
J Immunother Cancer. 2019 Apr 23;7(1):111. doi: 10.1186/s40425-019-0591-3.
5
Functional TRPV2 and TRPV4 channels in human cardiac c-kit(+) progenitor cells.人心脏c-kit(+)祖细胞中的功能性TRPV2和TRPV4通道
J Cell Mol Med. 2016 Jun;20(6):1118-27. doi: 10.1111/jcmm.12800. Epub 2016 Feb 10.
6
The polybasic lysine-rich domain of plasma membrane-resident STIM1 is essential for the modulation of store-operated divalent cation entry by extracellular calcium.质膜驻留型 STIM1 的多碱性赖氨酸富含结构域对于细胞外钙离子对钙库操纵性钙离子内流的调节是必需的。
Cell Signal. 2013 May;25(5):1328-37. doi: 10.1016/j.cellsig.2013.01.025. Epub 2013 Feb 8.
7
Extracellular ATP activates store-operated Ca entry in white adipocytes: functional evidence for STIM1 and ORAI1.细胞外 ATP 激活白色脂肪细胞中的储存操纵钙内流：STIM1 和 ORAI1 的功能证据。
Biochem J. 2018 Feb 14;475(3):691-704. doi: 10.1042/BCJ20170484.
8
FKBP52 is involved in the regulation of SOCE channels in the human platelets and MEG 01 cells.FKBP52参与人类血小板和MEG 01细胞中SOCE通道的调节。
Biochim Biophys Acta. 2013 Mar;1833(3):652-62. doi: 10.1016/j.bbamcr.2012.11.029. Epub 2012 Dec 8.
9
Conformation of ryanodine receptor-2 gates store-operated calcium entry in rat pulmonary arterial myocytes.兰尼碱受体-2的构象调控大鼠肺动脉平滑肌细胞中的钙库操纵性钙内流。
Cardiovasc Res. 2016 Jul 1;111(1):94-104. doi: 10.1093/cvr/cvw067. Epub 2016 Mar 24.
10
Assembly of ER-PM Junctions: A Critical Determinant in the Regulation of SOCE and TRPC1.内质网-质膜连接点的组装：在 SOCE 和 TRPC1 调节中的关键决定因素。
Adv Exp Med Biol. 2017;981:253-276. doi: 10.1007/978-3-319-55858-5_11.

引用本文的文献

1
Deletion of endothelial IGFBP5 protects against ischaemic hindlimb injury by promoting angiogenesis.内皮细胞 IGFBP5 的缺失通过促进血管生成来保护缺血性后肢损伤。
Clin Transl Med. 2024 Jun;14(6):e1725. doi: 10.1002/ctm2.1725.
2
NEDD4L is a promoter for angiogenesis and cell proliferation in human umbilical vein endothelial cells.NEDD4L 促进人脐静脉内皮细胞的血管生成和细胞增殖。
J Cell Mol Med. 2024 Apr;28(8):1-11. doi: 10.1111/jcmm.18233.
3
NMDARs antagonist MK801 suppresses LPS-induced apoptosis and mitochondrial dysfunction by regulating subunits of NMDARs via the CaM/CaMKII/ERK pathway.

本文引用的文献

1
TRPs and Ca in cell death and survival.TRP 通道与细胞死亡和存活过程中的钙离子。
Cell Calcium. 2018 Jan;69:4-18. doi: 10.1016/j.ceca.2017.07.002. Epub 2017 Jul 15.
2
Hypoxia modulates cell migration and proliferation in placenta-derived mesenchymal stem cells.缺氧调节胎盘间充质干细胞的迁移和增殖。
J Thorac Cardiovasc Surg. 2017 Aug;154(2):543-552.e3. doi: 10.1016/j.jtcvs.2017.03.141. Epub 2017 Apr 13.
3
Bradykinin regulates cell growth and migration in cultured human cardiac c-Kit+ progenitor cells.缓激肽调节培养的人心脏c-Kit+祖细胞的细胞生长和迁移。
N-甲基-D-天冬氨酸受体（NMDARs）拮抗剂MK801通过CaM/ CaMKII/ERK途径调节NMDARs亚基，从而抑制脂多糖（LPS）诱导的细胞凋亡和线粒体功能障碍。
Cell Death Discov. 2023 Feb 11;9(1):59. doi: 10.1038/s41420-023-01362-9.
4
Cryo-EM structures of human bradykinin receptor-G proteins complexes.人缓激肽受体-G 蛋白复合物的冷冻电镜结构。
Nat Commun. 2022 Feb 7;13(1):714. doi: 10.1038/s41467-022-28399-1.
5
Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis.刀豆球蛋白 A 通过 Akt/ERK/Cyclin D1 轴促进内皮细胞的血管生成和增殖。
Pharm Biol. 2022 Dec;60(1):65-74. doi: 10.1080/13880209.2021.2013259.
6
A modular map of Bradykinin-mediated inflammatory signaling network.缓激肽介导的炎症信号网络的模块化图谱。
J Cell Commun Signal. 2022 Jun;16(2):301-310. doi: 10.1007/s12079-021-00652-0. Epub 2021 Oct 29.
7
Pretreatment of cardiac progenitor cells with bradykinin attenuates HO-induced cell apoptosis and improves cardiac function in rats by regulating autophagy.预处理心脏祖细胞用缓激肽可通过调节自噬减轻 HO 诱导的细胞凋亡，改善大鼠心功能。
Stem Cell Res Ther. 2021 Aug 5;12(1):437. doi: 10.1186/s13287-021-02503-6.
Oncotarget. 2017 Feb 14;8(7):10822-10835. doi: 10.18632/oncotarget.14609.
4
TRPC1, Orai1, and STIM1 in SOCE: Friends in tight spaces.钙库操纵性钙内流中的瞬时受体电位通道蛋白1、Orai1和基质相互作用分子1：狭小空间中的伙伴
Cell Calcium. 2017 May;63:33-39. doi: 10.1016/j.ceca.2016.12.009. Epub 2016 Dec 30.
5
Preconditioning c-Kit-positive Human Cardiac Stem Cells with a Nitric Oxide Donor Enhances Cell Survival through Activation of Survival Signaling Pathways.用一氧化氮供体预处理c-Kit阳性人心脏干细胞可通过激活生存信号通路提高细胞存活率。
J Biol Chem. 2016 Apr 29;291(18):9733-47. doi: 10.1074/jbc.M115.687806. Epub 2016 Mar 3.
6
Functional TRPV2 and TRPV4 channels in human cardiac c-kit(+) progenitor cells.人心脏c-kit(+)祖细胞中的功能性TRPV2和TRPV4通道
J Cell Mol Med. 2016 Jun;20(6):1118-27. doi: 10.1111/jcmm.12800. Epub 2016 Feb 10.
7
Roles of store-operated Ca2+ channels in regulating cell cycling and migration of human cardiac c-kit+ progenitor cells.储存式钙通道在调节人类心脏c-kit+祖细胞的细胞周期和迁移中的作用。
Am J Physiol Heart Circ Physiol. 2015 Nov 15;309(10):H1772-81. doi: 10.1152/ajpheart.00260.2015. Epub 2015 Oct 9.
8
Ca(2+) signals mediated by bradykinin type 2 receptors in normal pancreatic stellate cells can be inhibited by specific Ca(2+) channel blockade.正常胰腺星状细胞中由缓激肽2型受体介导的Ca(2+)信号可被特异性Ca(2+)通道阻滞剂抑制。
J Physiol. 2016 Jan 15;594(2):281-93. doi: 10.1113/JP271468. Epub 2015 Nov 8.
9
Store-Operated Calcium Channels.储存式钙通道
Physiol Rev. 2015 Oct;95(4):1383-436. doi: 10.1152/physrev.00020.2014.
10
Effects of BKCa and Kir2.1 Channels on Cell Cycling Progression and Migration in Human Cardiac c-kit+ Progenitor Cells.大电导钙激活钾通道（BKCa）和内向整流钾通道2.1（Kir2.1）对人心脏c-kit+祖细胞细胞周期进程和迁移的影响
PLoS One. 2015 Sep 21;10(9):e0138581. doi: 10.1371/journal.pone.0138581. eCollection 2015.