Burns Alan J
Neural Development Unit, University College London Institute of Child Health, London, UK.
J Pediatr Gastroenterol Nutr. 2007 Dec;45 Suppl 2:S103-6. doi: 10.1097/MPG.0b013e31812e65e0.
Interstitial cells of Cajal (ICCs) have, in the past 2 decades, been recognised as important elements in the regulation of gastrointestinal motility. Specifically, they have been shown to be critical for the generation and propagation of electrical slow waves that regulate the phasic contractile activity of gastrointestinal smooth muscle, and for mediating neurotransmission from enteric motor neurons to smooth muscle cells. These different functional roles are carried out by different phenotypic classes of ICC that have discrete distributions within the tunica muscularis. Identifying the functional roles of ICC within the gut has been facilitated by studying mutant mice deficient in ICC, either as a consequence of loss of the tyrosine kinase receptor, Kit, or its ligand, stem cell factor, both of which are necessary for normal ICC development. In humans, under certain pathophysiological conditions, loss or defects in ICC networks appear to play a role in the generation of certain motility disorders. Alterations in ICC distribution have been reported in conditions such as achalasia, chronic intestinal pseudoobstruction, Hirschsprung disease, inflammatory bowel diseases, and slow transit constipation. Molecular and genetic techniques are helping researchers to determine whether defects in ICC networks are the cause of motility disorders, or whether the disrupted ICC networks are a consequence of gut dysfunction.
在过去20年里, Cajal间质细胞(ICC)已被公认为是胃肠运动调节中的重要元素。具体而言,它们已被证明对于调节胃肠平滑肌阶段性收缩活动的电慢波的产生和传播,以及介导从肠运动神经元到平滑肌细胞的神经传递至关重要。这些不同的功能作用由不同表型类别的ICC执行,它们在肌层内具有离散分布。通过研究ICC缺陷的突变小鼠,有助于确定ICC在肠道内的功能作用,这些突变小鼠要么是由于酪氨酸激酶受体Kit或其配体干细胞因子缺失所致,而这两者对于正常ICC发育都是必需的。在人类中,在某些病理生理条件下,ICC网络的缺失或缺陷似乎在某些运动障碍的发生中起作用。在诸如贲门失弛缓症、慢性肠道假性梗阻、先天性巨结肠、炎症性肠病和慢传输型便秘等病症中,已有ICC分布改变的报道。分子和基因技术正在帮助研究人员确定ICC网络缺陷是否是运动障碍的原因,或者被破坏的ICC网络是否是肠道功能障碍的结果。