Protein kinase C in the pancreatic acinar cell
Protein kinase C in the pancreatic acinar cell
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DOI：
10.1111/j.1440-1746.2007.05282.x
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发表时间：
2008-03-01
影响因子：
4.1
通讯作者：
Thrower, Edwin
中科院分区：
文献类型：
--
作者：
Gorelick, Fred;Pandol, Stephen;Thrower, Edwin
胰腺腺泡细胞内选择性信号分子的病理激活介导急性胰腺炎的发展。一些关键的早期腺泡细胞事件包括蛋白酶的激活、顶端分泌的抑制和炎症介质的产生。先前的研究表明，胆囊收缩素（CCK）的超生理浓度可引起体内胰腺炎，也会在分散的腺泡细胞（acini）群中引发这些病理反应。蛋白激酶 C (PKC) 调节许多细胞事件，并且该信号分子家族在胰腺炎的一些病理反应中的作用已被描述。值得注意的是，乙醇可以激活特定的 PKC 同工型，并使腺泡细胞对 CCK 的病理效应敏感。我们对分离的胰腺腺泡和无细胞重建系统的初步研究表明 PKC 可以介导腺泡细胞中的蛋白酶激活。这些发现可能与酒精和其他病因引起的胰腺炎的发病机制有关。
Pathological activation of selective signaling molecules within the pancreatic acinar cell mediates the development of acute pancreatitis. Some of the key early acinar cell events include activation of proteases, inhibition of apical secretion, and elaboration of inflammatory mediators. Previous studies have shown that supraphysiological concentrations of cholecystokinin (CCK) that can cause pancreatitis in vivo, also initiate these pathological responses in dispersed groups of acinar cells (acini). Protein kinase C (PKC) regulates many cellular events and a role for this family of signaling molecules has been described in some of the pathological responses of pancreatitis. Notably, ethanol can activate specific PKC isoforms and sensitize the acinar cells to the pathological effects of CCK. Our preliminary studies in isolated pancreatic acini and a cell-free reconstitution system suggest that PKC can mediate protease activation in the acinar cell. These findings may be relevant to the pathogenesis of pancreatitis from alcohol and other etiologies.