On the role of gap junctional communication in pancreatic acinar cell function

被引：0

作者：

Chanson, M ^{[1
]}

Jongsma, HJ ^{[1
]}

Mollard, P ^{[1
]}

Willecke, K ^{[1
]}

Suter, S ^{[1
]}

Meda, P ^{[1
]}

机构：

[1] Childrens Hosp, Dept Pediat, Geneva, Switzerland

来源：

GAP JUNCTIONS | 1998年

关键词：

D O I：

暂无

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The role of gap junctional communication in pancreatic acinar cell secretion is not understood. Using confocal digital imaging techniques and patch-clamp electrophysiology, we have found that junctional coupling provides for the intercellular diffusion of signaling molecules able to mobilize Ca2+ from internal stores which, in turn, stimulate exocytosis. This mechanism may contribute to the recruitement of pancreatic acinar cells to secrete in response to increasing doses of the Ca2+-mobilizing agonist acetylcholine (ACh). Maximal concentrations of ACh induced uncoupling of acinar cells, an effect that restricts the passage of Ca2+-signaling molecules and should be expected to attenuate stimulated secretion. However, pancreatic acinar cells from Cx32-deficient mice showed enhanced basal secretion as compared to control (coupled) acinar cells, a finding which is in agreement with the previous observation that enzyme release is increased during heptanol-mediated acinar cell uncoupling. Enhanced basal secretion during uncoupling may therefore represent a compensatory mechanism to sustain enzyme output. Such a mechanism would explain why acinar cell uncoupling induced by Ca2+-mobilizing agonists correlates with maximal secretory activity.

引用

页码：158 / 162

页数：5