ALTERATION OF INTESTINAL TIGHT JUNCTION STRUCTURE AND PERMEABILITY BY CYTOSKELETAL CONTRACTION
ALTERATION OF INTESTINAL TIGHT JUNCTION STRUCTURE AND PERMEABILITY BY CYTOSKELETAL CONTRACTION
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DOI：
10.1152/ajpcell.1987.253.6.c854
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发表时间：
1987-12-01
影响因子：
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通讯作者：
CARLSON, S
中科院分区：
文献类型：
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作者：
MADARA, JL;MOORE, R;CARLSON, S
通透性肠吸收细胞刷状缘含有肌动蛋白和肌球蛋白 (PAMR) 的连接周围环，可诱导其收缩。最近，表明在暴露于细胞松弛素D(CD)后回肠上皮的吸收细胞中发生暗示PAMR收缩的形态变化(J.Biol.102：2125-2136，1986)。通过这种反应，紧密连接结构也会发生改变，紧密连接渗透性也会增强。为了进一步评估 PAMR 收缩与增强的紧密连接通透性之间的关系，我们检查了解偶联剂 2,4-二硝基苯酚 (DNP) 对这种 CD 反应的影响。当 DNP 浓度为 0.1-1 mM 时，功能上定义的上皮内能量储存会逐渐耗尽。这样的 DNP 浓度不会独立损害紧密连接屏障功能。 CD暴露之前能量储存的耗尽消除了CD诱导紧密连接渗透性异常的能力。类似地，PAMR 凝结和紧密连接结构的改变可以通过功能能量储备的先前耗尽而与 CD 暴露分离。这些数据与 CD 引起了紧密连接结构和能量依赖性事件渗透性的改变，即 PAMR 内的张力调节紧密结构和功能。
Permeabilized intestinal absorptive cell brush borders contain a perijunctional ring of actin and myosin (PAMR) that can be induced to contract. Recently, morphological changes suggestive of PAMR contraction were shown to occur in absorptive cells of ileal epithelium after exposure to cytochalasin D (CD) (J. Biol. 102: 2125-2136, 1986). With this response, altered tight junction structure and enhanced tight junction permeability also occur. To further assess the relationship between PAMR contraction and enhanced tight junction permeability, we examined the effect of the uncoupler 2,4-dinitrophenol (DNP) on this CD response. Progressive depletion of functionally defined intraepithelial energy stores occurred with DNP concentrations of 0.1-1 mM. Such DNP concentrations did not independently impair tight junction barrier function. Depletion of energy stores before CD exposure ablated the ability of CD to induce abnormalities of tight juction permeability. Similarly, PAMR condensation and alteration in tight junction structure could be dissociated from CD exposure by prior depletion of functional energy reserves. These data tie CD elicited alterations in tight junction structure and permeability to an energy dependent event that tensile forces within the PAMR regulate tight structure and function.