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Critical role of ATP-induced ATP release for Ca2+ signaling in nonsensory cell networks of the developing cochlea | |
2016-11-15 | |
发表期刊 | PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (IF:9.4[JCR-2023],10.8[5-Year]) |
ISSN | 0027-8424 |
卷号 | 113期号:46页码:E7194-E7201 |
发表状态 | 已发表 |
DOI | 10.1073/pnas.1616061113 |
摘要 | Spatially and temporally coordinated variations of the cytosolic free calcium concentration ([Ca2+](c)) play a crucial role in a variety of tissues. In the developing sensory epithelium of the mammalian cochlea, elevation of extracellular adenosine trisphosphate concentration ([ATP](e)) triggers [Ca2+](c) oscillations and propagation of intercellular inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ waves. What remains uncertain is the relative contribution of gap junction channels and connexin hemichannels to these fundamental mechanisms, defects in which impair hearing acquisition. Another related open question is whether [Ca2+](c) oscillations require oscillations of the cytosolic IP3 concentration ([IP3](c)) in this system. To address these issues, we performed Ca2+ imaging experiments in the lesser epithelial ridge of the mouse cochlea around postnatal day 5 and constructed a computational model in quantitative adherence to experimental data. Our results indicate that [Ca2+](c) oscillations are governed by Hopf-type bifurcations within the experimental range of [ATP](e) and do not require [IP3](c) oscillations. The model replicates accurately the spatial extent and propagation speed of intercellular Ca2+ waves and predicts that ATP-induced ATP release is the primary mechanism underlying intercellular propagation of Ca2+ signals. The model also uncovers a discontinuous transition from propagating regimes (intercellular Ca2+ wave speed > 11 mu m.s(-1)) to propagation failure (speed = 0), which occurs upon lowering the maximal ATP release rate below a minimal threshold value. The approach presented here overcomes major limitations due to lack of specific connexin channel inhibitors and can be extended to other coupled cellular systems. |
关键词 | inositol trisphosphate calcium waves calcium oscillations cochlear nonsensory cells connexins |
收录类别 | SCI |
语种 | 英语 |
资助项目 | University of Padua[CPDR132235] |
WOS研究方向 | Science & Technology - Other Topics |
WOS类目 | Multidisciplinary Sciences |
WOS记录号 | WOS:000388970100009 |
出版者 | NATL ACAD SCIENCES |
WOS关键词 | GAP-JUNCTION CHANNELS ; INOSITOL 1,4,5-TRISPHOSPHATE DYNAMICS ; INNER-EAR ; CALCIUM OSCILLATIONS ; CONNEXIN 30 ; ENDOPLASMIC-RETICULUM ; ENDOTHELIAL-CELLS ; HEARING-LOSS ; GUINEA-PIG ; HEMICHANNELS |
原始文献类型 | Article |
引用统计 | 正在获取...
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文献类型 | 期刊论文 |
条目标识符 | https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/1639 |
专题 | 免疫化学研究所_特聘教授组_功能筛选实验室 |
通讯作者 | Pozzan, Tullio; Mammano, Fabio |
作者单位 | 1.Italian Natl Res Council, Inst Cell Biol & Neurobiol, Dept Biomed Sci, I-00015 Monterotondo, RM, Italy 2.Univ Padua, Dept Phys & Astron, I-35131 Padua, Italy 3.Fdn Adv Biomed Res, Venetian Inst Mol Med, Connexin Struct & Funct Unit, I-35129 Padua, Italy 4.Italian Natl Res Council, Inst Neurosci, Dept Biomed Sci, Padua Sect, I-35129 Padua, Italy 5.Univ Padua, Dept Biomed Sci, I-35121 Padua, Italy 6.ShanghaiTech Univ, Shanghai Inst Adv Immunochem Studies, Lab Phenotyp Screening, Shanghai 201210, Peoples R China |
通讯作者单位 | 免疫化学研究所 |
推荐引用方式 GB/T 7714 | Ceriani, Federico,Pozzan, Tullio,Mammano, Fabio. Critical role of ATP-induced ATP release for Ca2+ signaling in nonsensory cell networks of the developing cochlea[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,2016,113(46):E7194-E7201. |
APA | Ceriani, Federico,Pozzan, Tullio,&Mammano, Fabio.(2016).Critical role of ATP-induced ATP release for Ca2+ signaling in nonsensory cell networks of the developing cochlea.PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,113(46),E7194-E7201. |
MLA | Ceriani, Federico,et al."Critical role of ATP-induced ATP release for Ca2+ signaling in nonsensory cell networks of the developing cochlea".PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 113.46(2016):E7194-E7201. |
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