Journal articles: 'Transepithelial electrical resistance'

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Uematsu, Masafumi, Yasser Helmy Mohamed, Naoko Onizuka, Ryotaro Ueki, Daisuke Inoue, Azusa Fujikawa, Hitoshi Sasaki, and Takashi Kitaoka. "Less Invasive Corneal Transepithelial Electrical Resistance Measurement Method." Ocular Surface 14, no. 1 (January 2016): 37–42. http://dx.doi.org/10.1016/j.jtos.2015.07.004.

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Meyle, J., K. Guttig, G. Rascher, and H. Wolburg. "Transepithelial electrical resistance and tight junctions of human gingival keratinocvtes." Journal of Periodontal Research 34, no. 4 (May 1999): 214–22. http://dx.doi.org/10.1111/j.1600-0765.1999.tb02244.x.

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Rabito, C. A. "Reassembly of the occluding junctions in a renal cell line with characteristics of proximal tubular cells." American Journal of Physiology-Renal Physiology 251, no. 6 (December 1, 1986): F978—F987. http://dx.doi.org/10.1152/ajprenal.1986.251.6.f978.

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LLC-PK1 cells from trypsin-treated confluent cultures formed a continuous monolayer when plated at high cell density on collagen-coated Nuclepore filters. These monolayers developed a significant transepithelial electrical resistance that reached a maximum at 20 h. At 48 h, the resistance decreased to a value usually one-half the value obtained at 20 h. These changes were associated with an increase in the cell density of the monolayers. The drop in electrical resistance at 48 h was not observed when cell growth was arrested with excess thymidine. A hyperbolic relationship was demonstrated between cell density and electrical resistance. Although the increase in cell density was associated with an increase in the unidirectional flux of mannitol across the monolayers, selectivity studies indicated that the intrinsic properties of the occluding junctions were similar in the high and low cell density monolayers. These results indicate that, when cell growth is not arrested, changes in transepithelial electrical resistance observed after plating correspond to an increase in cell density and not to changes in the intrinsic properties of the occluding junctions. The development of transepithelial electrical resistance was delayed when the cells were in exponential growth. No such delay was observed, however, when exponential growth was synchronized. These findings and results obtained with the antimicrotubular agent Nocodazole indicate that the delay in the development of transepithelial electrical resistance is due to the asynchronous transit of the cells through the mitotic phase of the cell cycle: a time when most of the intercellular junctions are probably disrupted. Further investigation revealed that inhibition of protein but not mRNA synthesis blocked the development of occluding junctions in cells from confluent and exponentially growing cultures alike. These results indicate that, in contrast to MDCK cells, regulation of the occluding junctions in exponentially growing LLC-PK1 cells occurs at the translational not at the transcriptional level of protein synthesis.

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Velarde, G., S. Ait-Aissa, C. Gillet, F. Rogerieux, C. Lambre, E. Vindimian, and J. M. Porcher. "Use of Transepithelial Electrical Resistance in the Study of Pentachlorophenol Toxicity." Toxicology in Vitro 13, no. 4-5 (August 1999): 723–27. http://dx.doi.org/10.1016/s0887-2333(99)00048-x.

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Kaji, Hirokazu, Bibek Raut, and Takeshi Hori. "Realtime Transepithelial/Endothelial Electrical Resistance Measurements in Multiple Transwell Culture Inserts." ECS Meeting Abstracts MA2020-02, no. 44 (November 23, 2020): 2794. http://dx.doi.org/10.1149/ma2020-02442794mtgabs.

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Bataille, Amy M., James Goldmeyer, and J. Larry Renfro. "Avian renal proximal tubule epithelium urate secretion is mediated by Mrp4." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 6 (December 2008): R2024—R2033. http://dx.doi.org/10.1152/ajpregu.90471.2008.

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Birds are uricotelic and, like humans, maintain high plasma urate concentrations (∼300 μM). The majority of their urate waste, as in humans, is eliminated by renal proximal tubular secretion; however, the mechanism of urate transport across the brush-border membrane of the intact proximal tubule epithelium during secretion is uncertain. The dominance of secretory urate transport in the bird provides a convenient model for examining this process. The present study shows that short hairpin RNA interference (shRNAi) effectively knocked down gene expression of multidrug resistance protein 4 (Mrp4; 25% of control) in primary monolayer cultures of isolated chicken proximal tubule epithelial cells (cPTCs). Control and Mrp4-shRNAi-treated cPTCs were mounted in Ussing chambers and unidirectional transepithelial fluxes of urate were measured. To detect nonspecific effects, transepithelial electrical resistance (TER) and sodium-dependent glucose transport (Iglu) were monitored throughout experiments. Knocking down Mrp4 expression resulted in a reduction of transepithelial urate secretion to 35% of control with no effects on TER or Iglu. Although electrical gradient-driven urate transport in isolated brush-border membrane vesicles was confirmed, potassium-induced depolarization of the plasma membrane in intact cPTCs failed to inhibit active transepithelial urate secretion. However, electrical gradient-dependent vesicular urate transport was inhibited by the MRP4 inhibitor MK-571 also known to inhibit active transepithelial urate transport by cPTCs. Based on these data, direct measure of active transepithelial urate secretion in functional avian proximal tubule epithelium indicates that Mrp4 is the dominant apical membrane exit pathway from cell to lumen.

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Asgrimsson, Valthor, Thorarinn Gudjonsson, Gudmundur Hrafn Gudmundsson, and Olafur Baldursson. "Novel Effects of Azithromycin on Tight Junction Proteins in Human Airway Epithelia." Antimicrobial Agents and Chemotherapy 50, no. 5 (May 2006): 1805–12. http://dx.doi.org/10.1128/aac.50.5.1805-1812.2006.

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ABSTRACT The macrolide antibiotic azithromycin improves lung function and prognosis among patients with cystic fibrosis or diffuse panbronchiolitis, independently of bacterial eradication. Anti-inflammatory effects have been implicated, but data from in vivo studies are scarce, and the link between abnormal electrolyte content in airway surface liquid and bronchial infections remains uncertain. In the present study, we treated human airway epithelia on filter supports with azithromycin and monitored transepithelial electrical resistance. We found that azithromycin increased transepithelial electrical resistance of airway epithelia in a dose-dependent manner. Immunocytochemistry and Western blotting showed that addition of azithromycin changed the locations of proteins in cell cultures and induced processing of the tight junction proteins claudin-1 and claudin-4, occludin, and junctional adhesion molecule-A. These effects were reversible, and no effect was seen when cells were treated with penicillin or erythromycin. The data indicate that azithromycin increases the transepithelial electrical resistance of human airway epithelia by changing the processing of tight junction proteins. The results are novel and may help explain the beneficial effects of azithromycin in patients with cystic fibrosis, diffuse panbronchiolitis, and community-acquired pneumonia.

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Canil, C., I. Rosenshine, S. Ruschkowski, M. S. Donnenberg, J. B. Kaper, and B. B. Finlay. "Enteropathogenic Escherichia coli decreases the transepithelial electrical resistance of polarized epithelial monolayers." Infection and Immunity 61, no. 7 (1993): 2755–62. http://dx.doi.org/10.1128/iai.61.7.2755-2762.1993.

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Nicolas, A., F. Schavemaker, K. Kosim, D. Kurek, M. Haarmans, M. Bulst, K. Lee, et al. "High throughput transepithelial electrical resistance (TEER) measurements on perfused membrane-free epithelia." Lab on a Chip 21, no. 9 (2021): 1676–85. http://dx.doi.org/10.1039/d0lc00770f.

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We present an instrument for simultaneously measuring TEER in up to 80 perfused epithelial tubules on an OrganoPlate. The sensitivity, speed and ease of use enables screening of tubules during formation, drug exposure and inflammatory processes.

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Tafazoli, Farideh, Carl Q. Zeng, Mary K. Estes, Karl-Erik Magnusson, and Lennart Svensson. "NSP4 Enterotoxin of Rotavirus Induces Paracellular Leakage in Polarized Epithelial Cells." Journal of Virology 75, no. 3 (February 1, 2001): 1540–46. http://dx.doi.org/10.1128/jvi.75.3.1540-1546.2001.

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ABSTRACT The nonstructural NSP4 protein of rotavirus has been described as the first viral enterotoxin. In this study we have examined the effect of NSP4 on polarized epithelial cells (MDCK-1) grown on permeable filters. Apical but not basolateral administration of NSP4 was found to cause a reduction in the transepithelial electrical resistance, redistribution of filamentous actin, and an increase in paracellular passage of fluorescein isothiocyanate-dextran. Significant effects on transepithelial electrical resistance were noted after a 20- to 30-h incubation with 1 nmol of NSP4. Most surprisingly, the epithelium recovered its original integrity and electrical resistance upon removal of NSP4. Preincubation of nonconfluent MDCK-1 cells with NSP4 prevented not only development of a permeability barrier but also lateral targeting of the tight-junction-associated Zonula Occludens-1 (ZO-1) protein. Taken together, these data indicate new and specific effects of NSP4 on tight-junction biogenesis and show a novel effect of NSP4 on polarized epithelia.

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Finotti, Enrico, Riccardo Gezzi, Fabio Nobili, Ivana Garaguso, and Mendel Friedman. "Effect of apple, baobab, red-chicory, and pear extracts on cellular energy expenditure and morphology of a Caco-2 cells using transepithelial electrical resistance (TEER) and scanning electron microscopy (SEM)." RSC Advances 5, no. 29 (2015): 22490–98. http://dx.doi.org/10.1039/c4ra15129a.

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The present study investigated the effects of four food extracts on the Caco-2 intestinal cell line using a new transepithelial electrical resistance method (TEER) concurrent with electron microscopy (SEM).

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Bossink, Elsbeth G. B. M., Mariia Zakharova, Douwe S. de Bruijn, Mathieu Odijk, and Loes I. Segerink. "Measuring barrier function in organ-on-chips with cleanroom-free integration of multiplexable electrodes." Lab on a Chip 21, no. 10 (2021): 2040–49. http://dx.doi.org/10.1039/d0lc01289k.

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A cleanroom-free method to integrate electrodes for transepithelial/transendothelial electrical resistance (TEER) measurements in Organ-on-Chips (OoCs) is presented and validated for a gut and a blood-brain barrier model.

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Ludwig, Thomas, Rainer Ossig, Susanne Graessel, Marianne Wilhelmi, Hans Oberleithner, and Stefan W. Schneider. "The electrical resistance breakdown assay determines the role of proteinases in tumor cell invasion." American Journal of Physiology-Renal Physiology 283, no. 2 (August 1, 2002): F319—F327. http://dx.doi.org/10.1152/ajprenal.00327.2001.

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The electrical resistance breakdown of the Madin-Darby canine kidney (MDCK) cell monolayer provides a continuous assay system for cancer invasion that detects functional changes before morphological alterations. In this study, we address the question of whether physical contact between tumor cell and epithelial monolayer is a prerequisite for tumor cell invasion. When human melanoma cells were seeded directly (i.e., physical contact) on top of an electrically tight epithelial cell layer (5,800 ± 106 Ω · cm2), electrical monolayer leakage led to an 18 ± 3% reduction of transepithelial electrical resistance within 24 h. However, when melanoma cells were seeded close to the basolateral surface of the epithelial cell monolayer but separated by a filter membrane (i.e., no physical contact), electrical leakage occurred even more quickly (42 ± 3% reduction in 24 h). Atomic force microscopy detected discrete structural changes between cells. Electrical leakage was effectively blocked by α2-macroglobulin or ilomastat, inhibitors of matrix metalloproteinases. We conclude that exocytosis of soluble proteases causes electrical breakdown of the MDCK monolayer, independently of physical contact between tumor cells and the monolayer.

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Klingberg, Trine Danø, Maja Herold Pedersen, Avrelija Cencic, and Birgitte Bjørn Budde. "Application of Measurements of Transepithelial Electrical Resistance of Intestinal Epithelial Cell Monolayers To Evaluate Probiotic Activity." Applied and Environmental Microbiology 71, no. 11 (November 2005): 7528–30. http://dx.doi.org/10.1128/aem.71.11.7528-7530.2005.

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ABSTRACT Among five potentially probiotic lactobacilli investigated, Lactobacillus plantarum MF1298 and Lactobacillus salivarius DC5 showed the highest increase in the transepithelial electrical resistance (TER) of polarized monolayers of Caco-2 cells, and this increase was shown to be dose dependent. Furthermore, preincubation with MF1298 attenuated a decrease in TER induced by Listeria monocytogenes.

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Milks, L. C., G. P. Conyers, and E. B. Cramer. "The effect of neutrophil migration on epithelial permeability." Journal of Cell Biology 103, no. 6 (December 1, 1986): 2729–38. http://dx.doi.org/10.1083/jcb.103.6.2729.

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To reach an inflammatory lesion, neutrophils must frequently traverse the epithelium of an infected organ. Whether the actual migration of neutrophils alters the epithelial permeability is unknown. Through the use of an in vitro model system it was possible to directly determine the effect of neutrophil emigration on the transepithelial electrical resistance of the monolayer. Human neutrophils (5 X 10(6) cells/ml) were placed in the upper compartment of a combined chemotaxis/resistance chamber and stimulated for 40 min by a gradient of 10(-7) M n-formyl-methionyl-leucyl-phenylalanine to traverse a confluent monolayer of canine kidney epithelial cells grown on micropore filters. Neither the chemoattractant alone (10(-5)-10(-9) M) nor the accumulation of an average of eight neutrophils per millimeter of epithelium lowered the transepithelial electrical resistance. However, under certain conditions the migration of neutrophils temporarily increased the permeability of the monolayer. The resistance fell approximately 48% within 5 min if the migratory cells were stimulated to reverse their migration across the same monolayer. As re-migration continued, the resistance returned to its initial levels within 60 min. Doubling the initial neutrophil concentration to 10 X 10(6) cells/ml resulted in the accumulation of an average of 66 neutrophils per millimeter of epithelium and an average fall in resistance of 46% (r = 0.98; P less than 0.001) in 40 min. If the resistance had fallen less than 45%, removal of the neutrophils remaining in the upper compartment resulted in a return of the transepithelial electrical resistance to its initial level within 65 min. However, when the fall was greater than 45%, the resistance only recovered to 23.5% of its initial levels within the same time frame. Thus, these results suggest that the integrity of an epithelium can, under certain conditions, be affected by the emigration of neutrophils, but that this effect is either completely or partially reversible within 65 min.

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Leung, Lawrence W., Ruben G. Contreras, Catalina Flores-Maldonado, Marcelino Cereijido, and Enrique Rodriguez-Boulan. "Inhibitors of glycosphingolipid biosynthesis reduce transepithelial electrical resistance in MDCK I and FRT cells." American Journal of Physiology-Cell Physiology 284, no. 4 (April 1, 2003): C1021—C1030. http://dx.doi.org/10.1152/ajpcell.00149.2002.

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Madin-Darby canine kidney (MDCK) I and Fisher rat thyroid (FRT) cells exhibit transepithelial electrical resistance (TER) values in excess of 5,000 Ω · cm2. When these cells were incubated in the presence of various inhibitors of sphingolipid biosynthesis, a >5-fold reduction of TER was observed without changes in the gate function for uncharged solutes or the fence function for apically applied fluorescent lipids. The localization of ZO-1 and occludin was not altered between control and inhibitor-treated cells, indicating that the tight junction was still intact. Furthermore, the complexity of tight junction strands, analyzed by freeze-fracture microscopy, was not reduced. Once the inhibitor was removed and the cells were allowed to synthesize sphingolipids, a gradual recovery of the TER was observed. Interestingly, these inhibitors did not attenuate the TER of MDCK II cells, a cell line that typically exhibits values below 800 Ω · cm2. These results suggest that glycosphingolipids play a role in regulating the electrical properties of epithelial cells.

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Bajnath, R. B., M. H. van Hoeve, H. R. de Jonge, and J. A. Groot. "Regulation of apical Cl- conductance and basolateral K+ conductances by phorbol esters in HT-29cl.19A cells." American Journal of Physiology-Cell Physiology 263, no. 4 (October 1, 1992): C759—C766. http://dx.doi.org/10.1152/ajpcell.1992.263.4.c759.

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The effect of phorbol esters [4 beta-phorbol 12,13-dibutyrate (PDB) and phorbol 12-myristate 13-acetate (PMA)] on potential differences and resistances was studied with the conventional microelectrode technique applied to confluent filter-grown monolayers of the human colon carcinoma cell line HT-29cl.19A. Phorbol esters (PDB or PMA from 10(-7) to 10(-6) M) evoked 1) a transient increase in the transepithelial potential difference (peak value 3.5 +/- 0.5 mV), 2) a depolarization of the cell potential by 23 +/- 2 mV at the peak of the transepithelial potential change and a continued decrease during the decline of the transepithelial potential, and 3) a decrease of the fractional resistance of the apical membrane consisting of two phases, a relative rapid one (time constant 1.2 +/- 0.2 min) and a much slower further decrease during the second phase (time constant 34 +/- 1 min). Ion replacements and electrical circuit analyses indicate that PDB activates an apical Cl- conductance and slowly inhibits the basal K+ conductance of the basolateral membrane. PDB reduced the transepithelial response to forskolin due to inhibition of the basal K+ conductance. The Ca2+ ionophore ionomycin accelerated that effect of PDB. Staurosporine inhibited the effects of PDB, suggesting that the PDB effects are mediated via activation of a protein kinase C.

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Cho, Kyou-Nam, Stephen M. Becker, and Eric R. Houpt. "The NF-κB p50 Subunit Is Protective during Intestinal Entamoeba histolytica Infection of 129 and C57BL/6 Mice." Infection and Immunity 78, no. 4 (January 19, 2010): 1475–81. http://dx.doi.org/10.1128/iai.00669-09.

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ABSTRACT Entamoeba histolytica is the agent of amebic colitis. In this work we examined the intestinal NF-κB response to this parasite. Using an enzyme-linked immunosorbent assay (ELISA) and an electrophoretic mobility shift assay, we found that the NF-κB subunit p50 predominated in nuclear extracts of whole cecal tissue and of isolated crypts from mice inoculated with E. histolytica. p50 was protective, since C57BL/6 and 129 mice in which there was targeted deletion of this subunit were more susceptible to E. histolytica infection as measured by culture results, cecal parasite ELISA results, and/or histologic scores. The transepithelial electrical resistance of cecal explants from C57BL/6 and 129 p50 knockout mice decreased markedly in response to the parasite compared with the transepithelial electrical resistance of their wild-type counterparts, suggesting that a protective function of p50 was present in the epithelium itself. This work shows that NF-κB activity, particularly activity of the p50 subunit, is one factor that contributes to resistance of the gut to E. histolytica infection.

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McRoberts, J. A., and N. E. Riley. "Regulation of T84 cell monolayer permeability by insulin-like growth factors." American Journal of Physiology-Cell Physiology 262, no. 1 (January 1, 1992): C207—C213. http://dx.doi.org/10.1152/ajpcell.1992.262.1.c207.

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When grown on permeable supports, the T84 human colonic epithelial cell line forms polarized monolayer cultures with high-resistance tight junctions between adjacent cells. Addition of either insulin-like growth factor (IGF) I or II to the basolateral but not the apical membrane side of established monolayers caused a dose-dependent decrease in transepithelial resistance over a 4-day period. IGF-I was more potent than IGF-II, with half-maximally effective concentrations of 0.7 and 2.2 nM, respectively. Both IGF-I and -II caused a parallel increase in the transepithelial flux rates for Na+ and the extracellular space marker, mannitol, demonstrating that the decrease in electrical resistance was due to increased permeability through the tight junction-regulated paracellular pathway. Simultaneous addition of cycloheximide prevented the decline in electrical resistance, implying that protein synthesis is necessary for the effect of IGF on paracellular permeability. Treatment of monolayers with IGF produced a subtle condensation of the perijunctional actin ring as visualized using rhodamine-labeled phalloidin. These results demonstrate that IGF-I and -II regulate the paracellular permeability of T84 cell monolayers through a receptor-mediated process that probably involves changes in protein synthesis and cytoskeletal structure.

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Woodland, Philip, Chung-Yin Lee, Sean L. Preston, and Daniel Sifrim. "Tu1847 Esophageal Mucosa Dilated Intercellular Spaces (DIS), Transepithelial Electrical Resistance and Perception of Heartburn." Gastroenterology 144, no. 5 (May 2013): S—862. http://dx.doi.org/10.1016/s0016-5085(13)63204-7.

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Maoz, Ben M., Anna Herland, Olivier Y. F. Henry, William D. Leineweber, Moran Yadid, John Doyle, Robert Mannix, et al. "Organs-on-Chips with combined multi-electrode array and transepithelial electrical resistance measurement capabilities." Lab on a Chip 17, no. 13 (2017): 2294–302. http://dx.doi.org/10.1039/c7lc00412e.

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Yeste, J., X. Illa, C. Gutiérrez, M. Solé, A. Guimerà, and R. Villa. "Geometric correction factor for transepithelial electrical resistance measurements in transwell and microfluidic cell cultures." Journal of Physics D: Applied Physics 49, no. 37 (August 18, 2016): 375401. http://dx.doi.org/10.1088/0022-3727/49/37/375401.

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23

Madara, J. L., and K. Dharmsathaphorn. "Occluding junction structure-function relationships in a cultured epithelial monolayer." Journal of Cell Biology 101, no. 6 (December 1, 1985): 2124–33. http://dx.doi.org/10.1083/jcb.101.6.2124.

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Electrical circuit analysis was used to study the structural development of occluding junctions (OJs) in cultured monolayers composed to T84 cells. The magnitude of the increments in transepithelial resistance predicted by such analysis was compared with the magnitude of the measured increments in resistance. Confluent sheets of epithelial cells were formed after cells were plated at high density on collagen-coated filters. Using Claude's OJ strand count-resistance hypothesis (1978, J. Membr. Biol. 39:219-232), electrical circuit analysis of histograms describing OJ strand count distribution at different time points after plating predicted that junctional resistance should rise in a proportion of 1:21:50 from 18 h to 2 d to 5 d. This reasonably paralleled the degree of rise in transepithelial resistance over this period, which was 1:29:59. The ability to predict the observed resistance rise was eliminated if only mean strand counts were analyzed or if electrical circuit analysis of OJ strand counts were performed using an OJ strand count-resistance relationship substantially different from that proposed by Claude. Measurements of unidirectional fluxes of inulin, mannitol, and sodium indicated that restriction of transjunctional permeability accounted for the observed resistance rise, and that T84 junctional strands have finite permeability to molecules with radii less than or equal to 3.6 A but are essentially impermeable to molecules with radii greater than or equal to 15 A. The results suggest that general correlates between OJ structure and OJ ability to resist passive ion flow do exist in T84 monolayers. The study also suggests that such correlates can be obtained only if OJ structural data are analyzed as an electrical circuit composed of parallel resistors.

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Pannabecker, T. L., D. J. Aneshansley, and K. W. Beyenbach. "Unique electrophysiological effects of dinitrophenol in Malpighian tubules." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (September 1, 1992): R609—R614. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r609.

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In the course of electrophysiological studies of Malpighian tubules of the mosquito Aedes aegypti, we have found unusual effects of 2,4-dinitrophenol (DNP) that offer new insights into the electrogenic and conductive properties of the tubule. DNP (10(-4)M) depolarized the basolateral membrane voltage from -58.0 to -3.3 mV, and it depolarized the apical membrane voltage from 110.6 to 8.9 mV. In parallel the transepithelial electrical resistance increased from 11.4 to 16.8 k omega.cm, and the fractional resistance of the apical membrane increased from 0.32 to 0.57. On the assumption that measures of transepithelial resistance in the presence of DNP approach the shunt resistance, the experimental results indicate the following characteristics for the equivalent circuit of the tubule: 1) a shunt resistance that is approximately one-half the transcellular resistance, 2) low and high electromotive forces, respectively, at the basolateral and apical membranes of principal cells, 3) an electrogenic pump at the apical membrane, and 4) a basolateral membrane voltage that is due mostly to the voltage developed by current flow across the basolateral membrane resistance.

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McCarthy, K. M., I. B. Skare, M. C. Stankewich, M. Furuse, S. Tsukita, R. A. Rogers, R. D. Lynch, and E. E. Schneeberger. "Occludin is a functional component of the tight junction." Journal of Cell Science 109, no. 9 (September 1, 1996): 2287–98. http://dx.doi.org/10.1242/jcs.109.9.2287.

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Occludin's role in mammalian tight junction activity was examined by ‘labeling’ the occludin pool with immunologically detectable chick occludin. This was accomplished by first transfecting MDCK cell with the Lac repressor gene. HygR clones were then transfected with chick occludin cDNA inserted into a Lac operator construct. The resulting HygR/NeoR clones were plated on porous inserts and allowed to form tight junctions. Once steady state transepithelial electrical resistance was achieved, isopropyl- beta-D-thiogalactoside was added to induce chick occludin expression. Confocal laser scanning microscopy of monolayers immunolabeled with Oc-2 monoclonal antibody revealed that chick occludin localized precisely to the preformed tight junctions. When sparse cultures were maintained in low Ca2+ medium, chick occludin and canine ZO-1 co-localized to punctate sites in the cytoplasm suggesting their association within the same vesicular structures. In low calcium medium both proteins also co-localized to contact sites between occasional cell pairs, where a prominent bar was formed at the plasma membrane. Chick occludin was detectable by western blot within two hours of adding isopropyl- beta-D-thiogalactoside to monolayers that had previously achieved steady state transepithelial electrical resistance; this coincided with focal immunofluorescence staining for chick occludin at the cell membrane of some cells. A gradual rise in transepithelial electrical resistance, above control steady state values, began five hours after addition of the inducing agent reaching new steady state values, which were 30–40% above baseline, 31 hours later. Upon removal of isopropyl- beta-D-thiogalactoside chick occludin expression declined slowly until it was no longer detected in western blots 72 hours later; transepithelial electrical resistance also returned to baseline values during this time. While densitometric analysis of western blots indicated that the presence of chick occludin had no detectable effect on E-cadherin or ZO-1 expression, the possibility cannot be excluded that ZO-1 might be a limiting factor in the expression of chick occludin at the cell surface. To test whether expression of chick occludin affected the process of tight junction assembly, monolayers in low Ca2+ medium were treated with isopropyl- beta-D-thiogalactoside for 24 or 48 hours, before Ca2+ was added to stimulate tight junction assembly. Chick occludin did not alter the rate at which transepithelial electrical resistance developed, however, steady state values were 30–40% above control monolayers not supplemented with the inducing agent. By freeze fracture analysis, the number of parallel tight junction strands shifted from a mode of three in controls to four strands in cells expressing chick occludin and the mean width of the tight junction network increased from 175 +/- 11 nm to 248 +/- 16 nm. Two days after plating confluent monolayers that were induced to express chick occludin, mannitol flux was reduced to a variable degree relative to control monolayers. With continued incubation with the inducing agent, mannitol flux increased on day 11 to 50%, and TER rose to 45% above controls. Both of these changes were reversible upon removal of isopropyl- beta-D-thiogalactoside. These data are consistent with the notion that occludin contributes to the electrical barrier function of the tight junction and possibly to the formation of aqueous pores within tight junction strands.

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Duff, Tracey, Simon Carter, Gemma Feldman, Gordon McEwan, Walter Pfaller, Pauline Rhodes, Michael Ryan, and Gabrielle Hawksworth. "Transepithelial Resistance and Inulin Permeability as Endpoints in In Vitro Nephrotoxicity Testing." Alternatives to Laboratory Animals 30, no. 2_suppl (December 2002): 53–59. http://dx.doi.org/10.1177/026119290203002s08.

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Transepithelial electrical resistance (RT) and the flux of fluorescein isothiocyanate (FITC) across Madin Darby canine kidney (MDCK) strain 1 cells and porcine epithelial kidney (LLC-PK1) monolayers were compared between three laboratories for a range of nephrotoxins. The precision of the REMS AutoSampler was similar to that of the Ussing chamber and the ENDOHM® technique, but superior to using chopstick electrodes, for measurements of resistance. The nephrotoxins used were selective for the proximal tubule, and in all cases, LLC-PK1 cells were more sensitive than MDCK cells. In most cases, change in RT was a more sensitive indicator of damage than alterations in FITC flux. The REMS system provides high intra-plate precision for RT measurements and is a higher throughput system, which is applicable to screening for nephrotoxicity in vitro.

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Hirakata, Yoichi, Kohichi Izumikawa, Toshiyuki Yamaguchi, Shizunobu Igimi, Nobuhiko Furuya, Shigefumi Maesaki, Kazunori Tomono, et al. "Adherence to and Penetration of Human Intestinal Caco-2 Epithelial Cell Monolayers by Pseudomonas aeruginosa." Infection and Immunity 66, no. 4 (April 1, 1998): 1748–51. http://dx.doi.org/10.1128/iai.66.4.1748-1751.1998.

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ABSTRACT Clinical isolates of Pseudomonas aeruginosa from blood adhered to and penetrated intestinal Caco-2 cell monolayers to a greater degree than did isolates from sputum, with a concomitant drastic decrease in transepithelial electrical resistance. PAO-PR1, an avirulent exotoxin A mutant of PAO1, did not cause a decrease in the resistance. The Caco-2 monolayer system may be useful for the evaluation of certain P. aeruginosa virulence factor activities.

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DOLZER, JAN, STEFFI KRANNICH, KARIN FISCHER, and MONIKA STENGL. "OSCILLATIONS OF THE TRANSEPITHELIAL POTENTIAL OF MOTH OLFACTORY SENSILLA ARE INFLUENCED BY OCTOPAMINE AND SEROTONIN." Journal of Experimental Biology 204, no. 16 (August 15, 2001): 2781–94. http://dx.doi.org/10.1242/jeb.204.16.2781.

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SUMMARY The biogenic amine octopamine is known to enhance the sensitivity of male moths to their species-specific pheromones in flight-tunnel experiments. This sensitization of pheromone-guided upwind flight is at least partly due to octopamine-dependent increases in the peak nerve impulse frequency of the pheromone response of olfactory receptor neurons. It is not known, however,whether octopamine exerts its effects directly on the electrical properties of the olfactory receptor neurons or indirectly, via modulation of the accessory cells of the sensillum. In extracellular tip recordings of pheromone-dependent trichoid sensilla on the antennae of male Manduca sexta moths, we investigated the effects of octopamine and serotonin on the transepithelial potential, which is generated by the activity of V-ATPases in sensillar accessory cells. In addition, the action potential activity of unstimulated olfactory receptor neurons was examined in the presence of biogenic amines. Under constant environmental conditions, the transepithelial potential oscillated regularly with periods of 2-8 min and with a 1-25 mV peak-to-peak amplitude over periods of several hours. These oscillatory intervals were interrupted by periods of relatively stable transepithelial potential, correlated with flight activity by the moth. Octopamine reduced the amplitude of the transepithelial potential oscillation and decreased the resistance of the sensillum preparation in a dose-dependent manner. Serotonin altered the waveform of the transepithelial potential, but did not change the resistance of the preparation. Thus, both amines affect the accessory cells, but have different targets in the regulation of the transepithelial potential. Neither amine significantly influenced the spontaneous action potential activity of the olfactory receptor neurons.

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Alvarez, Lawrence J., Helen C. Turner, Aldo C. Zamudio, and Oscar A. Candia. "Serotonin-elicited inhibition of Cl− secretion in the rabbit conjunctival epithelium." American Journal of Physiology-Cell Physiology 280, no. 3 (March 1, 2001): C581—C592. http://dx.doi.org/10.1152/ajpcell.2001.280.3.c581.

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The effects of serotonin [5-hydroxytryptamine (5-HT)] on the transepithelial electrical properties of the short-circuited rabbit conjunctiva were examined. With this epithelium, the short-circuit current ( I sc) measures Cl− secretion plus an amiloride-resistant Na+ absorptive process. Apical addition of 5-HT (10 μM) elicited a prompt I screduction from 14.2 ± 1.2 to 10.9 ± 1.2 μA/cm2 and increased transepithelial resistance from 0.89 ± 0.05 to 1.03 ± 0.06 kΩ · cm2(means ± SE, n = 21, P < 0.05). Similar changes were obtained with conjunctivae bathed without Na+ in the apical bath, as well as with conjunctivae preexposed to bumetanide with the Cl−-dependent I sc sustained by the parallel activities of basolateral Na+/H+ and Cl−/HCO[Formula: see text] exchangers. In contrast, the 5-HT-evoked effects were attenuated by the absence of Cl−(Δ I sc = −0.5 ± 0.2, n = 5), suggesting that reduced Cl−conductance(s) is an effect of 5-HT exposure. In amphotericin B-treated conjunctiva and in the presence of a transepithelial K+gradient, 5-HT addition reduced K+ diffusion across the preparation by 13% and increased transepithelial resistance by 4% ( n = 6, P < 0.05), indicating that an inhibition in K+ conductance(s) was also detectable. Significant electrical responses also occurred under physiological conditions when 5-HT was introduced to epithelia pretreated with adrenergic agonists or protein kinase C, phospholipase C, phosphodiesterase, or adenylyl cyclase inhibitors or after perturbation of Ca2+ homeostasis. Briefly, the conjunctiva harbors the only known Cl−-secreting epithelium in which 5-HT evokes Cl− transport inhibition; receptor subtype and signal transduction mechanism were not determined.

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Clarke, H., A. P. Soler, and J. M. Mullin. "Protein kinase C activation leads to dephosphorylation of occludin and tight junction permeability increase in LLC-PK1 epithelial cell sheets." Journal of Cell Science 113, no. 18 (September 15, 2000): 3187–96. http://dx.doi.org/10.1242/jcs.113.18.3187.

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Activation of protein kinase C by exposure of LLC-PK1 renal epithelial cells to 10(−7) M TPA, a tumor promoting phorbol ester, results in a rapid and sustained increase in paracellular permeability as evidenced by a decrease in transepithelial electrical resistance. Occludin, the first identified transmembrane protein to be localized to the tight junction of both epithelial and endothelial cells is thought play an important role in tight junction barriers. Although transepithelial electrical resistance fell to less than 20% of initial values within 1 hour of TPA exposure, transmission electron microscopy showed no change in the gross morphology of the tight junction of cells treated with 10(−7) M TPA for up to 2 hours. Immunofluorescence microscopy revealed a more rapid change in the membrane distribution of ZO-1 compared to occludin in the TPA-treated cells. Immunoblot analysis indicated that occludin levels in total cell lysates as well as cytosolic, membrane (Triton-X soluble) and cytoskeletal (Triton-X insoluble) fractions remained unchanged for at least 2 hours in cells treated with 10(−7) M TPA compared to their corresponding control cells. As the phosphorylation state of occludin is thought to be important in both tight junction assembly and regulation, the effect of phorbol ester treatment on the phosphorylation of occludin was investigated. Surprisingly, activation of protein kinase C with 10(−7) M TPA resulted in a time-dependent decrease in threonine phosphorylation of occludin which correlated closely with the rapid decrease in transepithelial electrical resistance. This dephosphorylation of occludin, occurring after activation of a serine/threonine kinase by TPA, suggested that protein kinase C was not acting directly on this tight junction target protein. If occludin dephosphorylation is involved in increasing tight junction permeability, then protein kinase C is apparently further upstream in the signaling pathway regulating epithelial barrier function, with a downstream serine/threonine phosphatase acting upon occludin.

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Smyk, Paulina, Iga Hołyńska-Iwan, and Dorota Olszewska-Słonina. "Effect of Propolis Preparations on Transepithelial Electrical Potential, Resistance, and Ion Transport in In Vitro Study." Evidence-Based Complementary and Alternative Medicine 2019 (January 15, 2019): 1–9. http://dx.doi.org/10.1155/2019/3756092.

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Background. Propolis and its ethanol extract show positive germicidal, bacteriostatic, and anti-inflammatory antioxidants and regenerative properties after use on the surface of the skin. Propolis is in common use in production of cosmetics and in folk medicine. The influence of this resinous mixture on ion channels, channels located in skin cells membranes and skin electrical resistance, was not explained. Objective. The main aim of the study was the evaluation of electrophysiological skin parameters during mechanical and chemical-mechanical stimulation after use of ethanol extract of propolis and propolis ointment in comparison with iso-osmotic Ringer solution. Methods. Skin fragments were taken from white New Zealand rabbits and distributed into three experimental groups which were incubated in ethanol extract of propolis (EEP), propolis ointment, and Ringer solution. Then they were placed in a Ussing chamber to measure electrophysiological parameters values. Results. In this study the influence of EEP on changes in value of electrical potential during block of chloride ions transport at the same time was observed. Ethanol propolis extract dissolved in water increases the transepidermal sodium ions transport in contrast to propolis ointment. Conclusion. The way of preparation cosmetics, which contain propolis, has effects on transepidermal ions transport in the rabbit’s skin. The value of skin electrical resistance is changing with penetration depth of active propolis substances contained in cosmetics.

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Ashley, S. W., D. I. Soybel, L. De, and L. Y. Cheung. "Microelectrode studies of Necturus antral mucosa. II. Equivalent circuit analysis." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 5 (May 1, 1985): G574—G579. http://dx.doi.org/10.1152/ajpgi.1985.248.5.g574.

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Intracellular microelectrode techniques were employed to determine the equivalent circuit parameters in Necturus antral mucosa. Stable intracellular impalements were obtained using 15- to 50-M omega microelectrodes. Measured transepithelial and cellular potentials and voltage deflections produced by transepithelial current pulses were used to calculate the electrical resistances of the cell membranes and the equivalent electromotive forces (EMF) at both cell borders. The measured potentials were -4.1 +/- 0.8 mV for the entire epithelia, -41.8 +/- 5.1 mV for the apical membrane, and -45.9 +/- 5.0 mV for the basolateral membrane. Values for the resistances were 7,300 +/- 1,900 omega X cm2 for the apical, 3,990 +/- 1,170 omega X cm2 for the basolateral, and 710 +/- 40 omega X cm2 for the shunt. Assuming that the shunt EMF is zero with control Ringer solution on both sides of the tissue, the effect of this relatively low-resistance shunt on electrical parameters can be determined. The cell membrane EMFs are both oriented with the interior negative and are -1.2 +/- 9.7 mV (apical) and -69.7 +/- 11.3 mV (basolateral). The difference between these values and the measured potentials is the result of a flow of current through the shunt from serosa to mucosa, hyperpolarizing the apical and depolarizing the basolateral membranes.

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Hickman, James. "Transepithelial/endothelial Electrical Resistance (TEER) theory and applications for microfluidic body-on-a-chip devices." Journal of Rare Diseases Research & Treatment 1, no. 3 (November 1, 2016): 46–52. http://dx.doi.org/10.29245/2572-9411/2016/3.1026.

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Grumbach, Yael, Nga Vu Thi Quynh, Raphaël Chiron, and Valérie Urbach. "LXA4 stimulates ZO-1 expression and transepithelial electrical resistance in human airway epithelial (16HBE14o-) cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 1 (January 2009): L101—L108. http://dx.doi.org/10.1152/ajplung.00018.2008.

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Lipoxin A4 (LXA4) is a biologically active eicosanoid produced in human airways that displays anti-inflammatory properties. In cystic fibrosis and severe asthma, LXA4 production has been reported to be decreased, and, in such diseases, one of the consequences of airway inflammation is disruption of the tight junctions. In the present study, we investigated the possible role of LXA4 on tight junction formation, using transepithelial electrical resistance (TER) measurements, Western blotting, and immunofluorescence. We observed that exposure to LXA4 (100 nM) for 2 days significantly increased zonula occludens-1 (ZO-1), claudin-1, and occludin expression at the plasma membrane of confluent human bronchial epithelial 16HBE14o- cells. LXA4 (100 nM) stimulated the daily increase of the 16HBE14o- cell monolayer TER, and this effect was inhibited by boc-2 (LXA4 receptor antagonist). LXA4 also had a rapid effect on ZO-1 immunofluorescence at the plasma membrane and increased TER within 10 min. In conclusion, our experiments provide evidence that LXA4 plays certainly a new role for the regulation of tight junction formation and stimulation of the localization and expression of ZO-1 at the plasma membrane through a mechanism involving the LXA4 receptor.

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Woodland, P., C. Lee, and D. Sifrim. "PTU-162 Oesophageal Mucosal Dilated Intercellular Spaces (Dis), Transepithelial Electrical Resistance and Perception of Heartburn." Gut 62, Suppl 1 (June 2013): A114.3—A115. http://dx.doi.org/10.1136/gutjnl-2013-304907.252.

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Pell, Theresa J., Mike B. Gray, Sarah J. Hopkins, Richard Kasprowicz, James D. Porter, Tony Reeves, Wendy C. Rowan, et al. "Epithelial Barrier Integrity Profiling: Combined Approach Using Cellular Junctional Complex Imaging and Transepithelial Electrical Resistance." SLAS DISCOVERY: Advancing the Science of Drug Discovery 26, no. 7 (June 4, 2021): 909–21. http://dx.doi.org/10.1177/24725552211013077.

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A core aspect of epithelial cell function is barrier integrity. A loss of barrier integrity is a feature of a number of respiratory diseases, including asthma, allergic rhinitis, and chronic obstructive pulmonary disease. Restoration of barrier integrity is a target for respiratory disease drug discovery. Traditional methods for assessing barrier integrity have their limitations. Transepithelial electrical resistance (TEER) and dextran permeability methods can give poor in vitro assay robustness. Traditional junctional complex imaging approaches are labor-intensive and tend to be qualitative but not quantitative. To provide a robust and quantitative assessment of barrier integrity, high-content imaging of junctional complexes was combined with TEER. A scalable immunofluorescent high-content imaging technique, with automated quantification of junctional complex proteins zonula occludens-1 and occludin, was established in 3D pseudostratified primary human bronchial epithelial cells cultured at an air–liquid interface. Ionic permeability was measured using TEER on the same culture wells. The improvements to current technologies include the design of a novel 24-well holder to enable scalable in situ confocal cell imaging without Transwell membrane excision, the development of image analysis pipelines to quantify in-focus junctional complex structures in each plane of a Z stack, and the enhancement of the TEER data analysis process to enable statistical evaluation of treatment effects on barrier integrity. This novel approach was validated by demonstrating measurable changes in barrier integrity in cells grown under conditions known to perturb epithelial cell function.

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Parkos, CA, SP Colgan, C. Delp, MA Arnaout, and JL Madara. "Neutrophil migration across a cultured epithelial monolayer elicits a biphasic resistance response representing sequential effects on transcellular and paracellular pathways." Journal of Cell Biology 117, no. 4 (May 15, 1992): 757–64. http://dx.doi.org/10.1083/jcb.117.4.757.

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Migration of polymorphonuclear leukocytes across epithelia is a hallmark of many inflammatory disease states. Neutrophils traverse epithelia by migrating through the paracellular space and crossing intercellular tight junctions. We have previously shown (Nash, S., J. Stafford, and J.L. Madara. 1987. J. Clin. Invest. 80:1104-1113), that leukocyte migration across T84 monolayers, a model human intestinal epithelium, results in enhanced tight junction permeability--an effect quantitated by the use of a simple, standard electrical assay of transepithelial resistance. Here we show that detailed time course studies of the transmigration-elicited decline in resistance has two components, one of which is unrelated to junctional permeability. The initial decrease in resistance, maximal 5-13 min after initiation of transmigration, occurs despite inhibition of transmigration by an antibody to the common beta subunit of neutrophil beta 2 integrins, and is paralleled by an increase in transepithelial short-circuit current. Chloride ion substitution and inhibitor studies indicate that the early-phase resistance decline is not attributable to an increase in tight junction permeability but is due to decreased resistance across epithelial cells resulting from chloride secretion. Since T84 cells are accepted models for studies of the regulation of Cl- and water secretion, our results suggest that neutrophil transmigration across mucosal surfaces (for example, respiratory and intestinal tracts) may initially activate flushing of the surface by salt and water. Equally important, these studies, by providing a concrete example of sequential transcellular and paracellular effects on transepithelial resistance, highlight the fact that this widely used assay cannot simply be viewed as a direct functional probe of tight junction permeability.

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Sherman, Philip M., Kathene C. Johnson-Henry, Helen P. Yeung, Peter S. C. Ngo, Jacques Goulet, and Thomas A. Tompkins. "Probiotics Reduce Enterohemorrhagic Escherichia coli O157:H7- and Enteropathogenic E. coli O127:H6-Induced Changes in Polarized T84 Epithelial Cell Monolayers by Reducing Bacterial Adhesion and Cytoskeletal Rearrangements." Infection and Immunity 73, no. 8 (August 2005): 5183–88. http://dx.doi.org/10.1128/iai.73.8.5183-5188.2005.

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ABSTRACT The aim of this study was to determine if probiotics reduce epithelial injury following exposure to Escherichia coli O157:H7 and E. coli O127:H6. The pretreatment of intestinal (T84) cells with lactic acid-producing bacteria reduced the pathogen-induced drop in transepithelial electrical resistance. These findings demonstrate that probiotics prevent epithelial injury induced by attaching-effacing bacteria.

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Clark, Thomas M., Timothy K. Hayes, and Klaus W. Beyenbach. "Dose-dependent effects of CRF-like diuretic peptide on transcellular and paracellular transport pathways." American Journal of Physiology-Renal Physiology 274, no. 5 (May 1, 1998): F834—F840. http://dx.doi.org/10.1152/ajprenal.1998.274.5.f834.

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The mechanism of action of synthetic Culexcorticotropin-releasing factor (CRF)-like diuretic peptide (CCRF-DP) was investigated in isolated, perfused Malpighian tubules of the yellow fever mosquito, Aedes aegypti. Low concentrations of CCRF-DP (10−10 and 10−9 M) caused depolarizing oscillations of the lumen-positive transepithelial voltage ( V t) in Malpighian tubules, whereas high concentrations (10−8 and 10−7 M) first depolarized and then transiently hyperpolarized V t; CCRF-DP always lowered transepithelial resistance ( R t), regardless of voltage depolarization or hyperpolarization. The short-circuit current ( I sc), an electrical estimate of active transepithelial transport of Na and K, remained unchanged at low concentrations of CCRF-DP, but I sc more than doubled at high concentrations. These effects of CCRF-DP suggest dose-dependent sites of action: low concentrations of CCRF-DP affect the paracellular pathway, and high concentrations affect both paracellular and transcellular pathways.

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Rizzolo, L. J., and Z. Q. Li. "Diffusible, retinal factors stimulate the barrier properties of junctional complexes in the retinal pigment epithelium." Journal of Cell Science 106, no. 3 (November 1, 1993): 859–67. http://dx.doi.org/10.1242/jcs.106.3.859.

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The retinal pigment epithelium lies at the interface between the neural retina and the choriocapillaris where it forms a blood-retinal barrier. Barrier function requires a polarized distribution of plasma membrane proteins and ‘tight’ tight junctions. During chicken embryogenesis, these features develop gradually. Although terminal junctional complexes are established by embryonic day 4, the distribution of the Na+/K(+)-APTase is not polarized in all cells of the epithelium until embryonic day 11. Similarly, the tight junctions of early embryos are leaky, but become tight by hatching (embryonic day 21). We used primary cell culture to examine the molecular basis of this gradual induction of polarized function. Pigment epithelium harvested from embryonic day 7, and cultured on filters, formed monolayers coupled by junctional complexes. The distribution of the Na+/K(+)-ATPase was non-polarized and the tight junctions were leaky with a transepithelial electrical resistance of 20–30 omega cm2. To isolate diffusible factors that stimulate the transepithelial electrical resistance, neural retinas from embryonic day 7, 14 or 16 embryos were incubated at 37 degrees C in base medium for 6 hours. The conditioned medium was added to the apical chamber of freshly cultured pigment epithelium. The distribution of the Na+/K(+)-ATPase became basolateral, and the electrical resistance gradually increased two to three times over 6 days. The increase in electrical resistance corresponded to a decrease in the rate of [3H]inulin diffusion across the monolayer. The effectiveness of the conditioned medium increased steadily with increasing age of the neural retina. Rather than increased production of an active factor, apparently different active factors were produced at different ages.(ABSTRACT TRUNCATED AT 250 WORDS)

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Bekusova, Viktoria, Linda Droessler, Salah Amasheh, and Alexander G. Markov. "Effects of 1,2-Dimethylhydrazine on Barrier Properties of Rat Large Intestine and IPEC-J2 Cells." International Journal of Molecular Sciences 22, no. 19 (September 24, 2021): 10278. http://dx.doi.org/10.3390/ijms221910278.

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Colon cancer is accompanied by a decrease of epithelial barrier properties, which are determined by tight junction (TJ) proteins between adjacent epithelial cells. The aim of the current study was to analyze the expression of TJ proteins in a rat model of 1,2-dimethylhydrazine (DMH)-induced colorectal cancer, as well as the barrier properties and TJ protein expression of IPEC-J2 cell monolayers after incubation with DMH. Transepithelial electrical resistance and paracellular permeability for sodium fluorescein of IPEC-J2 were examined by an epithelial volt/ohm meter and spectrophotometry. The expression and localization of TJ proteins were analyzed by immunoblotting and immunohistochemistry. In the colonic tumors of rats with DMH-induced carcinogenesis, the expression of claudin-3 and -4 was significantly increased compared to controls. The transepithelial electrical resistance of IPEC-J2 cells increased, while paracellular permeability for sodium fluorescein decreased, accompanied by an increased expression of claudin-4. The increase of claudin-4 in rat colon after chronic DMH exposure was consistent with the acute effect of DMH on IPEC-J2 cells, which may indicate an essential role of this protein in colorectal cancer development.

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Francis, Stacy A., Joan M. Kelly, Joanne Mccormack, Rick A. Rogers, Jean Lai, Eveline E. Schneeberger, and Robert D. Lynch. "Rapid reduction of MDCK cell cholesterol by methyl-β-cyclodextrin alters steady state transepithelial electrical resistance." European Journal of Cell Biology 78, no. 7 (July 1999): 473–84. http://dx.doi.org/10.1016/s0171-9335(99)80074-0.

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Mukherjee, Tusharmouli, Emilio Squillantea, Marc Gillespieb, and Jun Shao. "Transepithelial Electrical Resistance is Not a Reliable Measurement of the Caco-2 Monolayer Integrity in Transwell." Drug Delivery 11, no. 1 (January 2004): 11–18. http://dx.doi.org/10.1080/10717540490280345.

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Muendoerfer, Marco, Ulrich F. Schaefer, Petra Koenig, Jutta S. Walk, Petra Loos, Stefan Balbach, Thomas Eichinger, and Claus-Michael Lehr. "Online monitoring of transepithelial electrical resistance (TEER) in an apparatus for combined dissolution and permeation testing." International Journal of Pharmaceutics 392, no. 1-2 (June 15, 2010): 134–40. http://dx.doi.org/10.1016/j.ijpharm.2010.03.046.

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Carmona-Hernandez, Juan Carlos, Gonzalo Taborda-Ocampo, Jonathan C. Valdez, Bradley W. Bolling, and Clara Helena González-Correa. "Polyphenol Extracts from Three Colombian Passifloras (Passion Fruits) Prevent Inflammation-Induced Barrier Dysfunction of Caco-2 Cells." Molecules 24, no. 24 (December 17, 2019): 4614. http://dx.doi.org/10.3390/molecules24244614.

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Chronic intestinal inflammation is associated with pathophysiology of obesity and inflammatory bowel diseases. Gastrointestinal inflammation increases barrier dysfunction exacerbating the immune response and perpetuating chronic inflammation. Anti-inflammatory flavonoids may prevent this intestinal barrier dysfunction. The purpose of this study was to evaluate the polyphenol composition of Colombian Passiflora edulis var. Flavicarpa (Maracuyá), Passiflora edulis var. Sims (Gulupa), and Passiflora ligularis var. Juss (Granadilla) (passion fruits) and to evaluate their ability to inhibit disruption of intestinal barrier dysfunction of Caco-2 (colorectal adenocarcinoma) cells by an inflammatory cocktail (IC). Polyphenols (flavan-3-ols, phenolic acids, flavonols), xanthenes, and a terpene were identified in passion fruits. Cyanidin 3-rutinoside, (+)-catechin and ferulic acid were the most abundant phenolics in P. edulis var. Flavicarpa, P. edulis var. Sims, and P. ligularis var. Juss, respectively. Fruit extracts prevented loss of transepithelial electrical resistance in Caco-2 cells treated with the IC. Among the extracts, P. ligularis var. Juss was most effective at maintaining Caco-2 transepithelial electrical resistance (TEER) with ~73% relative to the IC-treated cells with about 43% of initial TEER values. This fruit had cyanidin-3-rutinoside, (+)-catechin, (−)-epicatechin, and ferulic acid in its phenolic profile. Results of this work support the hypothesis that consumption of passion fruit extracts could benefit intestinal health.

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Isaacson, L., and S. Nicolson. "CONCEALED TRANSEPITHELIAL POTENTIALS AND CURRENT RECTIFICATION IN TSETSE FLY MALPIGHIAN TUBULES." Journal of Experimental Biology 186, no. 1 (January 1, 1994): 199–213. http://dx.doi.org/10.1242/jeb.186.1.199.

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1. Electrophysiological techniques have been applied to tsetse fly Malpighian tubules for the first time. 2. In either Cl- or SO42- Ringer, both non-perfused and perfused tubules displayed transtubular potentials (Vt) at or close to 0 mV. Exposure to cyclic AMP elicited a marked secretory response and, in SO42- Ringer, a sharp (lumen-positive) increase in Vt. In Cl- Ringer, despite more than double the secretory response, there was little or no change in Vt. 3. Replacing Cl- with SO42- Ringer, in the presence of cyclic AMP, promptly increased Vt. In perfused tubules, this occurred irrespective of the Cl- or SO42- composition of the perfusate. 4. In Cl- Ringer, the transepithelial resistance (Rtrans) was less than half that previously reported in Malpighian tubules of other species. Cyclic AMP reduced Rtrans still further, whether tubules were bathed in Cl- or SO42- Ringer. 5. Currentvoltage (I/V) plots often displayed current rectification, both before and more frequently after exposure to cyclic AMP, thus permitting estimation of both the electromotive force of the Na+ transport mechanism (ENa) and of the shunt resistance (Rshunt). Both ENa and Rshunt were markedly lower in tubules bathed in Cl- than in SO42- Ringer. Cyclic AMP was without effect on ENa and Rshunt, in either Cl- or SO42- Ringer. 6. In terms of the equivalent electrical circuit, the secretory response to cyclic AMP was due solely to a fall in resistance of the active transport pathway (Rseries). The absence of an appreciable Vt, in Cl- Ringer, is consistent with an apical Cl- shunt.

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Demarest, J. R., and T. E. Machen. "Microelectrode measurements from oxyntic cells in intact Necturus gastric mucosa." American Journal of Physiology-Cell Physiology 249, no. 5 (November 1, 1985): C535—C540. http://dx.doi.org/10.1152/ajpcell.1985.249.5.c535.

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The electrical properties of oxyntic cells were measured in intact isolated Necturus fundic mucosa by dissecting away the serosal muscle and connective tissue and impaling the oxyntic cells across their basolateral membranes. Their properties under resting [i.e., not secreting acid (10(-4) M serosal cimetidine)] and stimulated (10(-4) M histamine) conditions were compared with those of surface cells impaled across their apical membranes in a separate set of experiments. Histamine hyperpolarized the transepithelial potential by 6-10 mV and reduced the transepithelial resistance by approximately 40%. The basolateral membrane potential (Vcs) of both cell types was significantly hyperpolarized by histamine, that of oxyntic cells from a resting value of -50 to -59 mV (P less than 0.001) and that of surface cells from -50 to -54 mV (P less than 0.05). Histamine also hyperpolarized the apical membrane potential (Vmc) of the oxyntic cells; however, the Vmc of surface cells was significantly depolarized. The ratio of the apical to basolateral cell membrane resistances Ra/Rb (delta Vmc/delta Vcs resulting from transepithelial current pulses) of resting oxyntic cells was 1.1 and that of surface cells was 3.6. Stimulation did not affect the Ra/Rb of either cell type. A tenfold increase in serosal K+ concentration depolarized Vcs and increased Ra/Rb of resting and stimulated oxyntic cells, indicating a significant basolateral K+ conductance. The results are consistent with a purely passive role for surface cells and indicate that stimulation results in a simultaneous decrease of both the apical and basolateral membrane resistances of the oxyntic cells.

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Yu, Alan S. L., Karin M. McCarthy, Stacy A. Francis, Joanne M. McCormack, Jean Lai, Rick A. Rogers, Robert D. Lynch, and Eveline E. Schneeberger. "Knockdown of occludin expression leads to diverse phenotypic alterations in epithelial cells." American Journal of Physiology-Cell Physiology 288, no. 6 (June 2005): C1231—C1241. http://dx.doi.org/10.1152/ajpcell.00581.2004.

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The function of occludin (Occ) in the tight junction is undefined. To gain insight into its role in epithelial cell biology, occludin levels in Madin-Darby canine kidney II cells were suppressed by stably expressing short interfering RNA. Suppression of occludin was associated with a decrease in claudins-1 and -7 and an increase in claudins-3 and -4. Claudin-2 levels were unaffected. The tight junction “fence” function was not impaired in suppressed Occ (Occ−) clones, as determined by BODIPY-sphingomyelin diffusion in the membrane. The most striking changes were those related to control of the cytoskeleton and the “gate” function of tight junctions. A reduced ability of Occ− clones to extrude apoptotic cells from the monolayers suggested that neighbors of apoptotic cells either failed to sense their presence or were unable to coordinate cytoskeletal activity necessary for their extrusion. To further test the extent to which actin cytoskeletal activity depends on the presence of occludin, Occ− and Occ+ monolayers were depleted of cholesterol. Previous studies showed that cholesterol depletion is associated with reorganization of the actin cytoskeleton and a fall in transepithelial electrical resistance. In contrast to control Occ (Occ+) cells, transepithelial electrical resistance did not fall significantly in cholesterol-depleted Occ− monolayers and they failed to generate Rho-GTP, one of the signaling molecules involved in regulating the actin cytoskeleton. While steady-state transepithelial electrical resistance was similar in all clones, tight junction permeability to mono- and divalent inorganic cations was increased in Occ− monolayers. In addition, there was a disproportionately large increase in permeability to monovalent organic cations, up to 6.96 Å in diameter. Chloride permeability was unaffected and there was little change in mannitol flux. The data suggest that occludin transduces external (apoptotic cells) and intramembrane (rapid cholesterol depletion) signals via a Rho signaling pathway that, in turn, elicits reorganization of the actin cytoskeleton. Impaired signaling in the absence of occludin may also alter the dynamic behavior of tight junction strands, as reflected by an increase in permeability to large organic cations; the permeability of ion pores formed of claudins, however, is less affected.

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Alexander, Frank, Sebastian Eggert, and Joachim Wiest. "Skin-on-a-Chip: Transepithelial Electrical Resistance and Extracellular Acidification Measurements through an Automated Air-Liquid Interface." Genes 9, no. 2 (February 21, 2018): 114. http://dx.doi.org/10.3390/genes9020114.

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Hasegawa, Hiroshi, Hirotada Fujita, Hironori Katoh, Junko Aoki, Kazuhiro Nakamura, Atsushi Ichikawa, and Manabu Negishi. "Opposite Regulation of Transepithelial Electrical Resistance and Paracellular Permeability by Rho in Madin-Darby Canine Kidney Cells." Journal of Biological Chemistry 274, no. 30 (July 23, 1999): 20982–88. http://dx.doi.org/10.1074/jbc.274.30.20982.

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Journal articles on the topic 'Transepithelial electrical resistance'

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