Energy dependence of restitution in the gastric mucosa
Energy dependence of restitution in the gastric mucosa
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DOI：
10.1152/ajpcell.2001.281.2.c430
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发表时间：
2001-08-01
影响因子：
5.5
通讯作者：
Hagen, SJ
中科院分区：
文献类型：
--
作者：
Cheng, AM;Morrison, SW;Hagen, SJ
损伤后的快速上皮修复(恢复)是维持胃肠道粘膜和皮肤屏障功能所必需的，被认为是一个高度依赖于ATP的过程，在低氧条件下会受到抑制。然而，人们对修复所需的代谢途径知之甚少。因此，本研究在体外评估氧化呼吸和糖酵解在损伤后修复中的作用。为此，在以下条件下对牛蛙胃粘膜的修复进行了评估：1)阻断线粒体呼吸；2)阻断糖酵解；或3)缺乏葡萄糖。通过电生理学和形态学评价损伤后粘膜修复的程度。线粒体呼吸受阻时发生细胞迁移、复极化和损伤后紧密连接的形成，而粘膜屏障功能未恢复。相反，糖酵解抑制通过抑制表面上皮细胞的迁移，完全阻断了修复的所有方面。在用无葡萄糖溶液孵育的组织中发生了修复，这表明细胞含有足够的葡萄糖(糖原)来驱动糖酵解数小时。我们的结果表明，糖酵解途径对于牛蛙胃粘膜损伤后的修复是必不可少的，并且在没有线粒体呼吸的情况下，屏障功能几乎完全修复。
Rapid epithelial repair (restitution) after injury is required to maintain barrier function of the gastrointestinal mucosa and skin and is thought to be a highly ATP-dependent process that would be inhibited under hypoxic conditions. However, little is known about the metabolic pathways required for restitution. Thus, this study was undertaken to evaluate, in vitro, the role of oxidative respiration and glycolysis in restitution after injury. To this end, restitution of the bullfrog gastric mucosa was evaluated under the following conditions: 1) blockade of mitochondrial respiration; 2) blockade of glycolysis; or 3) absence of glucose. The extent of mucosal repair after injury was evaluated by electrophysiology and morphology. Cell migration, repolarization, and the formation of tight junctions after injury occurred during blockade of mitochondrial respiration, whereas the recovery of mucosal barrier function did not. In contrast, glycolytic inhibition completely blocked all aspects of restitution by inhibiting the migration of surface epithelial cells. Restitution occurred in tissues incubated with glucose-free solutions, suggesting that cells contain sufficient glucose (glycogen) to drive glycolysis for many hours. Our results demonstrate that the glycolytic pathway is essential for restitution after injury in the bullfrog gastric mucosa and that all but complete repair of barrier function occurs in the absence of mitochondrial respiration.