Mooseker M S, Keller T C, Hirokawa N
Ciba Found Symp. 1983;95:195-215. doi: 10.1002/9780470720769.ch12.
Calcium plays a vital part in the regulation of cytoskeletal structure and contractility in the brush border of intestinal epithelial cells. An increased Ca2+ concentration causes a rapid but reversible solation of microvillar core filaments, which is mediated by an actin-'severing' protein of the core (Mr = 95 000), referred to as MV-95 K or villin. Results of recent experiments on the Ca2+-dependent interaction of MV-95 K with actin are summarized, and various functions for this actin-severing protein in the intestinal epithelial cell are discussed. Calcium also regulates contractility in the brush border, as shown by studies of isolated brush borders in vitro from chicken intestine. In the presence of Ca2+ (greater than 1 microM) and ATP (at 37 degrees C) isolated brush borders dramatically contract, over 1-4 min, via an isometric contraction of the terminal web region, similar to that observed by R. Rodewald on neonatal rat brush borders. This contraction is mediated, at least in part, by contraction of the circumferential bundle of actin filaments that are associated with the zonula adherens and may also involve myosin-mediated contractions between adjacent microvillar rootlets. Analysis of Ca2+-dependent phosphorylation of brush border proteins during terminal web contraction demonstrates a simultaneous phosphorylation of the regulatory light chain of brush border myosin. Like contraction, the brush border myosin kinase is activated by free Ca2+ (greater than 1 microM) and is inhibited by trifluoperazine, an inhibitor of calmodulin function. These results demonstrate that the machinery required for both production and regulation of force are integral components of the brush border cytostructure.
钙在调节肠上皮细胞刷状缘的细胞骨架结构和收缩性方面起着至关重要的作用。钙离子浓度升高会导致微绒毛核心细丝迅速但可逆地溶解,这是由核心的一种肌动蛋白“切割”蛋白(分子量 = 95000)介导的,该蛋白被称为MV-95K或绒毛蛋白。总结了近期关于MV-95K与肌动蛋白的钙依赖性相互作用的实验结果,并讨论了这种肌动蛋白切割蛋白在肠上皮细胞中的各种功能。钙还调节刷状缘的收缩性,这在体外从鸡肠道分离的刷状缘研究中得到了证实。在存在钙离子(大于1微摩尔)和ATP(在37摄氏度)的情况下,分离的刷状缘会在1-4分钟内通过终末网区域的等长收缩而显著收缩,类似于R.罗德瓦尔德在新生大鼠刷状缘上观察到的情况。这种收缩至少部分是由与紧密连接相关的肌动蛋白丝周向束的收缩介导的,也可能涉及相邻微绒毛小根之间肌球蛋白介导的收缩。对终末网收缩过程中刷状缘蛋白的钙依赖性磷酸化分析表明,刷状缘肌球蛋白的调节轻链同时发生磷酸化。与收缩一样,刷状缘肌球蛋白激酶被游离钙离子(大于1微摩尔)激活,并被钙调蛋白功能抑制剂三氟拉嗪抑制。这些结果表明,产生和调节力所需的机制是刷状缘细胞结构的组成部分。