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胰腺星状细胞中的钙信号传导:机制与潜在作用

Calcium signalling in pancreatic stellate cells: Mechanisms and potential roles.

作者信息

Gryshchenko Oleksiy, Gerasimenko Julia V, Gerasimenko Oleg V, Petersen Ole H

机构信息

Medical Research Council Group, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK; Bogomoletz Institute of Physiology, Kiev 01024, Ukraine.

Medical Research Council Group, Cardiff School of Biosciences, Cardiff University, Cardiff CF10 3AX, Wales, UK.

出版信息

Cell Calcium. 2016 Mar;59(2-3):140-4. doi: 10.1016/j.ceca.2016.02.003. Epub 2016 Feb 28.

DOI:10.1016/j.ceca.2016.02.003
PMID:26960936
Abstract

Hepatic and pancreatic stellate cells may or may not be regarded as stem cells, but they are capable of remarkable transformations. There is less information about stellate cells in the pancreas than in the liver, where they were discovered much earlier and therefore have been studied longer and more intensively than in the pancreas. Most of the work on pancreatic stellate cells has been carried out in studies on cell cultures, but in this review we focus attention on Ca(2+) signalling in stellate cells in their real pancreatic environment. We review current knowledge on patho-physiologically relevant Ca(2+) signalling events and their underlying mechanisms. We focus on the effects of bradykinin in the initial stages of acute pancreatitis, an often fatal disease in which the pancreas digests itself and its surroundings. Ca(2+) signals, elicited in the stellate cells by the action of bradykinin, may have a negative effect on the outcome of the acute disease process and promote the development of chronic pancreatitis. The bradykinin-elicited Ca(2+) signals can be inhibited by blockade of type 2 receptors and also by blockade of Ca(2+)-release activated Ca(2+) channels. The potential benefits of such pharmacological inhibition for the treatment of pancreatitis are reviewed.

摘要

肝星状细胞和胰腺星状细胞可能被视为干细胞,也可能不被视为干细胞,但它们能够发生显著的转变。与肝脏相比,关于胰腺星状细胞的信息较少,肝脏中的星状细胞发现得更早,因此比胰腺中的星状细胞研究得更久、更深入。大多数关于胰腺星状细胞的研究是在细胞培养实验中进行的,但在本综述中,我们将注意力集中在真实胰腺环境中星状细胞的钙(Ca2+)信号传导上。我们综述了关于病理生理相关的钙信号事件及其潜在机制的现有知识。我们重点关注缓激肽在急性胰腺炎初始阶段的作用,急性胰腺炎是一种常致命的疾病,胰腺会自我消化及其周围组织。缓激肽作用于星状细胞引发的钙信号可能对急性疾病进程的结果产生负面影响,并促进慢性胰腺炎的发展。缓激肽引发的钙信号可通过阻断2型受体以及阻断钙释放激活钙通道来抑制。本文综述了这种药物抑制对胰腺炎治疗的潜在益处。

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