Calcium waving from the pancreas: the physiological regulation of cytosolic Ca2+ signals in vivo.
Calcium waving from the pancreas: the physiological regulation of cytosolic Ca2+ signals in vivo.
复制标题
来自胰腺的钙波：体内胞质 Ca2 信号的生理调节。
DOI：
10.1113/jp284674
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Bruce JIE
中科院分区：
文献类型：
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作者：
Bruce JIE
在发现时空Ca2+信号传导方面有许多范式转变的技术进步，其中胰腺腺泡细胞处于这些发现的最前沿。多年来，人们认为激动剂诱导的胞质Ca 2+反应包括峰值和平台反应。直到1986年，Peter Cobbold和他的同事才首次使用显微注射的水母发光蛋白（Ca 2+敏感生物发光蛋白）测量了激动剂诱导的单个肝细胞胞浆Ca 2+振荡（Woods等人，1986年）。这是一个真正的范式转变的发现，并导致了研究的爆炸充分表征复杂的时间特性的Ca2+信号响应于不同的激动剂在多种细胞类型。在急性分离的胰腺腺泡细胞，激素胆囊收缩素（CCK）诱导的特征缓慢基线Ca2+振荡，而迷走神经释放的神经递质乙酰胆碱（ACh）诱导叠加在升高的基线上的快速Ca2+振荡（Yule等人，1991年）。随着成像显微镜的空间和时间分辨率的提高，这些激动剂诱导的Ca 2+振荡被证明局限于胰腺腺泡细胞的顶端区域（Thorn等人，1993年）。在接下来的几年里，关于乙酰胆碱和胆囊收缩素诱发的钙离子信号的特征性机制有很多争论，包括
There have been numerous paradigmshifting technological advances in the discovery of spatiotemporal Ca2+ signalling with pancreatic acinar cells being at the forefront of these discoveries. For many years it was thought that agonist-induced cytosolic Ca2+ responses comprised a peak and plateau response. It was not until 1986 that Peter Cobbold and his co-workers first measured agonist-induced cytosolic Ca2+ oscillations in single hepatocytes, using microinjected aequorin (Ca2+-sensing bioluminescent protein)(Woods et al., 1986). This was a truly paradigm-shifting discovery and led to an explosion of research fully characterizing the complex temporal properties of Ca2+ signalling in response to different agonists in multiple cell types.In acutely isolated pancreatic acinar cells, the hormone cholecystokinin (CCK) induced characteristic slow baseline Ca2+ oscillations, whereas the vagally released neurotransmitter acetylcholine(ACh) induced rapid Ca2+ oscillations superimposed over a raised baseline (Yule et al., 1991). As the spatial and temporal resolution of imaging microscopy improved, these agonist-induced Ca2+ oscillations were shown to be localized to the apical region of pancreatic acinar cells (Thorn et al., 1993). Over the following years there was much debate as to the mechanisms underlying the characteristic ACh-and CCK-evoked Ca2+ signals, including