Van Driessche Willy, Kreindler James L, Malik Asrar B, Margulies Susan, Lewis Simon A, Kim Kwang-Jin
Laboratory of Physiology, Campus Gasthuisberg O&N, K.U. Leuven, Leuven, Belgium.
Am J Physiol Lung Cell Mol Physiol. 2007 Sep;293(3):L520-4. doi: 10.1152/ajplung.00218.2007. Epub 2007 Jun 29.
In this synopsis of a symposium at EB2007, we start with an overview of noise and impedance analyses that have been applied to various epithelial barriers. Noise analysis yields specific information about ion channels and their regulation in epithelial and endothelial barriers. Impedance analysis can yield information about apical and basolateral membrane conductances and paracellular conductance of both epithelial and endothelial barriers. Using a morphologically based model, impedance analysis has been used to assess changes in apical and basolateral membrane surface areas and dimensions of the lateral intercellular space. Impedance analysis of an in vitro airway epithelial barrier under normal, nucleotide-stimulated, and cigarette smoke-exposed conditions yielded information on how activation and inhibition of secretion occur in airway epithelial cells. Similarly, impedance analysis of primary rat alveolar epithelial cell monolayer model under control and EGTA exposure conditions indicate that EGTA causes decreases in resistances of tight junctional routes as well as apical and basolateral cell membranes without causing much change in cell capacitances. In a stretch-caused injury model of alveolar epithelium, transcellular ion transport function and paracellular permeability of solute transport appear to be differentially regulated. Finally, inhibition of caveolae-mediated transcytosis in lung endothelium led to disruption of paracellular routes, increasing the physical dimension and permeability of tight junctional region. These data together demonstrate the cross talk between transcellular and paracellular transport (function and routes) of lung epithelial and endothelial barriers. Mechanistic (e.g., signaling cascades) information on such cross talk remain to be determined.
在本次关于EB2007研讨会的概述中，我们首先对已应用于各种上皮屏障的噪声和阻抗分析进行概述。噪声分析可得出有关上皮和内皮屏障中离子通道及其调节的特定信息。阻抗分析可得出有关上皮和内皮屏障的顶端和基底外侧膜电导以及细胞旁电导的信息。利用基于形态学的模型，阻抗分析已被用于评估顶端和基底外侧膜表面积以及细胞间外侧间隙尺寸的变化。在正常、核苷酸刺激和香烟烟雾暴露条件下对体外气道上皮屏障进行阻抗分析，得出了气道上皮细胞中分泌激活和抑制如何发生的信息。同样，在对照和EGTA暴露条件下对原代大鼠肺泡上皮细胞单层模型进行阻抗分析表明，EGTA会导致紧密连接途径以及顶端和基底外侧细胞膜的电阻降低，而细胞电容变化不大。在肺泡上皮拉伸损伤模型中，跨细胞离子转运功能和溶质转运的细胞旁通透性似乎受到不同调节。最后，抑制肺内皮细胞中小窝介导的转胞吞作用会导致细胞旁途径破坏，增加紧密连接区域的物理尺寸和通透性。这些数据共同证明了肺上皮和内皮屏障的跨细胞和细胞旁转运（功能和途径）之间的相互作用。关于这种相互作用的机制（例如信号级联）信息仍有待确定。
