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Journal articles on the topic 'Claudin-5'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Kiuchi-Saishin, Yumiko, Shimpei Gotoh, Mikio Furuse, Akiko Takasuga, Yasuo Tano, and Shoichiro Tsukita. "Differential Expression Patterns of Claudins, Tight Junction Membrane Proteins, in Mouse Nephron Segments." Journal of the American Society of Nephrology 13, no. 4 (2002): 875–86. http://dx.doi.org/10.1681/asn.v134875.

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ABSTRACT. As the first step in understanding the physiologic functions of claudins (tight junction integral membrane proteins) in nephrons, the expression of claudin-1 to -16 in mouse kidneys was examined by Northern blotting. Among these claudins, only claudin-6, -9, -13, and -14 were not detectable. Claudin-5 and -15 were detected only in endothelial cells. Polyclonal antibodies specific for claudin-7 and -12 were not available. Therefore, the distributions of claudin-1, -2, -3, -4, -8, -10, -11, and -16 in nephron segments were examined with immunofluorescence microscopy. For identification

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2

Jakab, Csaba, Judit Halász, Attila Szász, et al. "Expression and localisation of claudin-1,-2,-3,-4,-5,-7 and-10 proteins in the normal canine mammary gland." Acta Veterinaria Hungarica 56, no. 3 (2008): 341–52. http://dx.doi.org/10.1556/avet.56.2008.3.8.

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The recently identified claudins are dominant components of tight junctions, responsible for cell adhesion, polarity and paracellular permeability. Certain claudins have been shown to have relevance in tumour development. The aim of the present study was to analyse the expression of claudin-1,-2,-3,-4,-5,-7 and-10 in normal canine mammary glands. Samples from the inguinal mammary regions of 20 non-castrated, 1–13 years old female dogs were studied. Immunohistochemical analysis was performed on conventional specimens and tissue microarrays. The results of the immunohistochemical reactions detec

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Markov, Alexander G., Arina A. Fedorova, Violetta V. Kravtsova, et al. "Circulating Ouabain Modulates Expression of Claudins in Rat Intestine and Cerebral Blood Vessels." International Journal of Molecular Sciences 21, no. 14 (2020): 5067. http://dx.doi.org/10.3390/ijms21145067.

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The ability of exogenous low ouabain concentrations to affect claudin expression and therefore epithelial barrier properties was demonstrated previously in cultured cell studies. We hypothesized that chronic elevation of circulating ouabain in vivo can affect the expression of claudins and tight junction permeability in different tissues. We tested this hypothesis in rats intraperitoneally injected with ouabain (1 μg/kg) for 4 days. Rat jejunum, colon and brain frontal lobes, which are variable in the expressed claudins and tight junction permeability, were examined. Moreover, the porcine jeju

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4

Ahn, C., D. Lee, and E. B. Jeung. "216 HORMONAL REGULATION OF CLAUDIN-4 TIGHT JUNCTION MOLECULE IN MOUSE PLACENTA." Reproduction, Fertility and Development 27, no. 1 (2015): 198. http://dx.doi.org/10.1071/rdv27n1ab216.

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Tight junctions (TJ) are composed of a branching network of sealing strands. TJ regulate paracellular conductance and ionic selectivity. TJ components include the peripheral protein ZO-1, junctional adhesion molecules (JAM) and the integral proteins such as occludin and claudin. Claudins are a family of proteins that are the most important components in the tight junctions. The established paracellular transport barriers that control transportation of molecules within intercellular space. The present study focused on the expression of claudin, suggesting as major working molecules in the parac

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5

Daugherty, Brandy L., Madalina Mateescu, Anand S. Patel, et al. "Developmental regulation of claudin localization by fetal alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (2004): L1266—L1273. http://dx.doi.org/10.1152/ajplung.00423.2003.

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Tight junction proteins in the claudin family regulate epithelial barrier function. We examined claudin expression by human fetal lung (HFL) alveolar epithelial cells cultured in medium containing dexamethasone, 8-bromo-cAMP, and isobutylmethylxanthanine (DCI), which promotes alveolar epithelial cell differentiation to a type II phenotype. At the protein level, HFL cells expressed claudin-1, claudin-3, claudin-4, claudin-5, claudin-7, and claudin-18, where levels of expression varied with culture conditions. DCI-treated differentiated HFL cells cultured on permeable supports formed tight trans

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6

Chen, Stephen P., Beiyun Zhou, Brigham C. Willis, et al. "Effects of transdifferentiation and EGF on claudin isoform expression in alveolar epithelial cells." Journal of Applied Physiology 98, no. 1 (2005): 322–28. http://dx.doi.org/10.1152/japplphysiol.00681.2004.

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Rat alveolar epithelial type II cells grown on polycarbonate filters form high-resistance monolayers and concurrently acquire many phenotypic properties of type I cells. Treatment with EGF has previously been shown to increase transepithelial resistance across alveolar epithelial cell (AEC) monolayers. We investigated changes in claudin expression in primary cultured AEC during transdifferentiation to the type I cell-like phenotype ( days 0, 1, and 8), and on day 5 in culture ± EGF (10 ng/ml) from day 0 or day 4. Claudins 4 and 7 were increased, whereas claudins 3 and 5 were decreased, on late

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7

Ohta, Hiromitsu, Shigeki Chiba, Masahito Ebina, Mikio Furuse, and Toshihiro Nukiwa. "Altered expression of tight junction molecules in alveolar septa in lung injury and fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 2 (2012): L193—L205. http://dx.doi.org/10.1152/ajplung.00349.2010.

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The dysfunction of alveolar barriers is a critical factor in the development of lung injury and subsequent fibrosis, but the underlying molecular mechanisms remain poorly understood. To clarify the pathogenic roles of tight junctions in lung injury and fibrosis, we examined the altered expression of claudins, the major components of tight junctions, in the lungs of disease models with pulmonary fibrosis. Among the 24 known claudins, claudin-1, claudin-3, claudin-4, claudin-7, and claudin-10 were identified as components of airway tight junctions. Claudin-5 and claudin-18 were identified as com

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8

András, Ibolya E., Hong Pu, Jing Tian, et al. "Signaling Mechanisms of HIV-1 Tat-Induced Alterations of Claudin-5 Expression in Brain Endothelial Cells." Journal of Cerebral Blood Flow & Metabolism 25, no. 9 (2005): 1159–70. http://dx.doi.org/10.1038/sj.jcbfm.9600115.

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Exposure of brain microvascular endothelial cells (BMEC) to human immunodeficiency virus-1 (HIV-1) Tat protein can decrease expression and change distribution of tight junction proteins, including claudin-5. Owing to the importance of claudin-5 in maintaining the blood–brain barrier (BBB) integrity, the present study focused on the regulatory mechanisms of Tat-induced alterations of claudin-5 mRNA and protein levels. Real-time reverse-transcription-polymerase chain reaction revealed that claudin-5 mRNA was markedly diminished in BMEC exposed to Tat. However, U0126 (an inhibitor of mitogen-acti

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9

Abuazza, Ghazala, Amy Becker, Scott S. Williams, et al. "Claudins 6, 9, and 13 are developmentally expressed renal tight junction proteins." American Journal of Physiology-Renal Physiology 291, no. 6 (2006): F1132—F1141. http://dx.doi.org/10.1152/ajprenal.00063.2006.

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The adult proximal tubule is a low-resistance epithelium where there are high rates of both active transcellular and passive paracellular NaCl transport. We have previously demonstrated that the neonatal rabbit and rat proximal tubule have substantively different passive paracellular transport properties than the adult proximal tubule, which results in a maturational change in the paracellular passive flux of ions. Neonatal proximal tubules have a higher PNa/PCl ratio and lower chloride and bicarbonate permeabilities than adult proximal tubules. Claudins are a large family of proteins which ar

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10

Ahn, C., J. S. Lee, and E. B. Jeung. "128 EXPRESSIONS OF MOUSE TIGHT JUNCTION MOLECULES IN PLACENTA – CLAUDINS AND OTHER PARACELLULAR TRANSPORT MOLECULES." Reproduction, Fertility and Development 26, no. 1 (2014): 178. http://dx.doi.org/10.1071/rdv26n1ab128.

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Tight junctions (TJ) are composed of a branching network of sealing strands. Tight junctions regulate paracellular conductance and ionic selectivity. The TJ components include the peripheral protein ZO-1, junctional adhesion molecules (JAM), and integral proteins, such as occludin and claudin. Claudins, a family of proteins, are the most important components in TJ. They establish paracellular transport barriers, which control transportation of molecules within intercellular space. The current study focused on expression of claudin, suggesting claudin as a major working molecule in the paracell

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11

Gowrikumar, Saiprasad, Mark Primeaux, Kristina Pravoverov, et al. "A Claudin-Based Molecular Signature Identifies High-Risk, Chemoresistant Colorectal Cancer Patients." Cells 10, no. 9 (2021): 2211. http://dx.doi.org/10.3390/cells10092211.

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Identifying molecular characteristics that are associated with aggressive cancer phenotypes through gene expression profiling can help predict treatment responses and clinical outcomes. Claudins are deregulated in colorectal cancer (CRC). In CRC, increased claudin-1 expression results in epithelial-to-mesenchymal transition and metastasis, while claudin-7 functions as a tumor suppressor. In this study, we have developed a molecular signature based on claudin-1 and claudin-7 associated with poor patient survival and chemoresistance. This signature was validated using an integrated approach incl

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12

Kage, Hidenori, Per Flodby, Danping Gao, et al. "Claudin 4 knockout mice: normal physiological phenotype with increased susceptibility to lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 7 (2014): L524—L536. http://dx.doi.org/10.1152/ajplung.00077.2014.

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Claudins are tight junction proteins that regulate paracellular ion permeability of epithelium and endothelium. Claudin 4 has been reported to function as a paracellular sodium barrier and is one of three major claudins expressed in lung alveolar epithelial cells (AEC). To directly assess the role of claudin 4 in regulation of alveolar epithelial barrier function and fluid homeostasis in vivo, we generated claudin 4 knockout (Cldn4 KO) mice. Unexpectedly, Cldn4 KO mice exhibited normal physiological phenotype although increased permeability to 5-carboxyfluorescein and decreased alveolar fluid

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13

Jakab, Csaba, Miklós Rusvai, Péter Gálfi, Ágnes Szabára, Zoltán Szabó, and Janina Kulka. "Immunohistochemical detection of arteriolar hyperplasia in canine liver biopsy samples using the claudin-5 antibody." Acta Veterinaria Hungarica 58, no. 4 (2010): 423–30. http://dx.doi.org/10.1556/avet.58.2010.4.3.

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Claudins are key tight junctional proteins between adjacent epithelial, mesothelial or endothelial cells, which are responsible for the permeability of the paracellular space. This paper describes that the endothelial cells of normal hepatic arterioles, portal venules and portal lymphatics as well as the endothelium of sinusoids from dogs show strong membranous claudin-5 cross-reactivity. In 25 liver biopsy samples taken from dogs with portal vein hypoperfusion, an increased number of arterioles was detected in the portal areas (PAs) by the use of humanised anti-claudin-5 antibody. The increas

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14

Törzsök, Péter, Péter Riesz, István Kenessey, et al. "Claudins and Ki-67." Journal of Histochemistry & Cytochemistry 59, no. 11 (2011): 1022–30. http://dx.doi.org/10.1369/0022155411424606.

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Updated classification of urothelial cell cancer differentiates low-grade and high-grade cancers, which determines potential clinical outcome. Substantial interobserver variability necessitates new biomarkers to ensure classification. Claudins’ specific expression pattern characterizes normal tissues, different tumor types, and defined grades of tumor differentiation. The aim of this study was to examine the expression pattern of claudins and proliferation marker Ki-67 in low-grade and high-grade urothelial cell cancers compared with independent control samples of non-tumorous urothelium, as w

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15

Morita, Kazumasa, Hiroyuki Sasaki, Mikio Furuse, and Shoichiro Tsukita. "Endothelial Claudin." Journal of Cell Biology 147, no. 1 (1999): 185–94. http://dx.doi.org/10.1083/jcb.147.1.185.

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Tight junctions (TJs) in endothelial cells are thought to determine vascular permeability. Recently, claudin-1 to -15 were identified as major components of TJ strands. Among these, claudin-5 (also called transmembrane protein deleted in velo-cardio-facial syndrome [TMVCF]) was expressed ubiquitously, even in organs lacking epithelial tissues, suggesting the possible involvement of this claudin species in endothelial TJs. We then obtained a claudin-6–specific polyclonal antibody and a polyclonal antibody that recognized both claudin-5/TMVCF and claudin-6. In the brain and lung, immunofluoresce

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Beggs, Megan R., Ida Appel, Per Svenningsen, Karsten Skjødt, R. Todd Alexander, and Henrik Dimke. "Expression of transcellular and paracellular calcium and magnesium transport proteins in renal and intestinal epithelia during lactation." American Journal of Physiology-Renal Physiology 313, no. 3 (2017): F629—F640. http://dx.doi.org/10.1152/ajprenal.00680.2016.

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Significant alterations in maternal calcium (Ca2+) and magnesium (Mg2+) balance occur during lactation. Ca2+ is the primary divalent cation mobilized into breast milk by demineralization of the skeleton and alterations in intestinal and renal Ca2+ transport. Mg2+ is also concentrated in breast milk, but the underlying mechanisms are not well understood. To determine the molecular alterations in Ca2+ and Mg2+ transport in the intestine and kidney during lactation, three groups of female mice consisting of either nonpregnant controls, lactating mice, or mice undergoing involution were examined.

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17

Rossa, Jan, Jonas Protze, Christian Kern, et al. "Molecular and structural transmembrane determinants critical for embedding claudin-5 into tight junctions reveal a distinct four-helix bundle arrangement." Biochemical Journal 464, no. 1 (2014): 49–60. http://dx.doi.org/10.1042/bj20140431.

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A model of the transmembrane arrangement of claudin-5 as a prototype claudin is provided. Claudin subtype-specific molecular interfaces formed by conserved coiled-coil motifs and non-conserved residues in distinct positions of TM3/TM4 and ECL2 of claudin-5 essentially contribute to claudin-5 assembly into tight junctions.

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18

Morrow, Carla M. K., Dolores Mruk, C. Yan Cheng, and Rex A. Hess. "Claudin and occludin expression and function in the seminiferous epithelium." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1546 (2010): 1679–96. http://dx.doi.org/10.1098/rstb.2010.0025.

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Integral membrane proteins that contribute to function of the blood–testes barrier (BTB) in mice include claudins 3, 5 and 11 and occludin. Although claudin 11 is expressed throughout all stages of the seminiferous epithelial cycle, claudins 3 and 5 have specific expression at stage VIII. These differences in protein expression suggest that the interactions among, and functions of, these integral membrane proteins may shift over the course of the seminiferous epithelial cycle. Also, differences in expression among rodent species and men may make interpretation of studies across species challen

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LaFemina, Michael J., Deepti Rokkam, Anita Chandrasena, et al. "Keratinocyte growth factor enhances barrier function without altering claudin expression in primary alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 299, no. 6 (2010): L724—L734. http://dx.doi.org/10.1152/ajplung.00233.2010.

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Keratinocyte growth factor (KGF) has efficacy in several experimental models of lung injury; however, the mechanisms underlying KGF's protective effect remain incompletely understood. This study was undertaken to determine whether KGF augments barrier function in primary rat alveolar epithelial cells grown in culture, specifically whether KGF alters tight junction function via claudin expression. KGF significantly increased alveolar epithelial barrier function in culture as assessed by transepithelial electrical resistance (TER) and paracellular permeability. Fluorescence-activated cell sortin

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Wen, Huajie, Debbie D. Watry, M. Cecilia G. Marcondes, and Howard S. Fox. "Selective Decrease in Paracellular Conductance of Tight Junctions: Role of the First Extracellular Domain of Claudin-5." Molecular and Cellular Biology 24, no. 19 (2004): 8408–17. http://dx.doi.org/10.1128/mcb.24.19.8408-8417.2004.

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ABSTRACT Claudin-5 is a protein component of many endothelial tight junctions, including those at the blood-brain barrier, a barrier that limits molecular exchanges between the central nervous system and the circulatory system. To test the contribution of claudin-5 to this barrier function of tight junctions, we expressed murine claudin-5 in Madin-Darby canine kidney II cells. The result was a fivefold increase in transepithelial resistance in claudin-5 transductants and a reduction in conductance of monovalent cations. However, the paracellular flux of neither neutral nor charged monosacchari

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Coyne, Carolyn B., Todd M. Gambling, Richard C. Boucher, Johnny L. Carson, and Larry G. Johnson. "Role of claudin interactions in airway tight junctional permeability." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 5 (2003): L1166—L1178. http://dx.doi.org/10.1152/ajplung.00182.2003.

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Airway epithelial tight junctions (TJs) serve to separate the external and internal environments of the lung. However, the members of the claudin family that mediate this function have not been fully delineated. We characterized the claudin expression in normal airways removed from human donors during lung transplantation and determined the contribution of each claudin to airway barrier function. Stable cell lines in NIH/3T3 and human airway (IB3.1) cells were constructed expressing the claudin components found in the human airway, claudin-1, -3, or -5. The effects of claudin expression on tra

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Jakab, Csaba, Miklós Rusvai, Péter Gálfi, Judit Halász, and Janina Kulka. "Expression of claudin-5 in canine pancreatic acinar cell carcinoma — An immunohistochemical study." Acta Veterinaria Hungarica 59, no. 1 (2011): 87–98. http://dx.doi.org/10.1556/avet.59.2011.1.8.

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Claudin-5 is an endothelium-specific tight junction protein. The aim of the present study was to detect the expression pattern of this molecule in intact pancreatic tissues and in well-differentiated and poorly differentiated pancreatic acinar cell carcinomas from dogs by the use of cross-reactive humanised anticlaudin-5 antibody. The necropsy samples taken from dogs included 10 nonneoplastic pancreatic tissues, 10 well-differentiated pancreatic acinar cell carcinomas, 10 poorly differentiated pancreatic acinar cell carcinomas, 5 intrahepatic metastases of well-differentiated and 5 intrahepati

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Poliak, Sebastian, Sean Matlis, Christoph Ullmer, Steven S. Scherer, and Elior Peles. "Distinct claudins and associated PDZ proteins form different autotypic tight junctions in myelinating Schwann cells." Journal of Cell Biology 159, no. 2 (2002): 361–72. http://dx.doi.org/10.1083/jcb.200207050.

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The apposed membranes of myelinating Schwann cells are joined by several types of junctional specializations known as autotypic or reflexive junctions. These include tight, gap, and adherens junctions, all of which are found in regions of noncompact myelin: the paranodal loops, incisures of Schmidt-Lanterman, and mesaxons. The molecular components of autotypic tight junctions have not been established. Here we report that two homologues of Discs Lost–multi PDZ domain protein (MUPP)1, and Pals-associated tight junction protein (PATJ), are differentially localized in myelinating Schwann cells an

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Hering, Fromm, Bücker, et al. "Tilivalline- and Tilimycin-Independent Effects of Klebsiella oxytoca on Tight Junction-Mediated Intestinal Barrier Impairment." International Journal of Molecular Sciences 20, no. 22 (2019): 5595. http://dx.doi.org/10.3390/ijms20225595.

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Abstract: Klebsiella oxytoca causes antibiotic-associated hemorrhagic colitis and diarrhea. This was attributed largely to its secreted cytotoxins tilivalline and tilimycin, inductors of epithelial apoptosis. To study whether Klebsiella oxytoca exerts further barrier effects, T84 monolayers were challenged with bacterial supernatants derived from tilivalline/tilimycin-producing AHC6 or its isogeneic tilivalline/tilimycin-deficient strain Mut-89. Both preparations decreased transepithelial resistance, enhanced fluorescein and FITC-dextran-4kDa permeabilities, and reduced expression of barrier-f

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Geng, P., T. Ma, J. Xing, et al. "Dexamethasone ameliorates H2S-induced acute lung injury by increasing claudin-5 expression via the PI3K pathway." Human & Experimental Toxicology 37, no. 6 (2017): 626–35. http://dx.doi.org/10.1177/0960327117721961.

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Acute lung injury (ALI) is a major outcome of exposure to high levels of hydrogen sulfide (H2S). Dexamethasone (DXM) has been used to treat ALI. However, the mechanisms involved in H2S-induced ALI and the protective mechanisms of DXM in treating ALI are still nebulous. To explore the mechanisms involved, we evaluated the role of claudin-5 in the protective effect of DXM against H2S-induced ALI. Sprague-Dawley rats were exposed to H2S to establish the ALI model. In parallel with the animal model, a cell model was also established by incubating human umbilical vein endothelial cells (HUVECs) wit

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Luissint, Anny-Claude, Christian Federici, François Guillonneau та ін. "Guanine Nucleotide-Binding Protein Gαi2: A New Partner of Claudin-5 that Regulates Tight Junction Integrity in Human Brain Endothelial Cells". Journal of Cerebral Blood Flow & Metabolism 32, № 5 (2012): 860–73. http://dx.doi.org/10.1038/jcbfm.2011.202.

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The blood—brain barrier (BBB) selectively controls the exchanges between the blood and the brain: it is formed by tight junctions (TJs) between adjacent microvascular endothelial cells. The transmembrane protein claudin-5 is known as a key TJ protein at the BBB, although, the molecular mechanisms by which it regulates TJ tightness are poorly understood. To identify putative claudin-5 partners that contribute to TJ integrity, claudin-5-enriched membrane microdomains were prepared by cell fractionation, using the human brain endothelial cell line hCMEC/D3 and claudin-5 immunoprecipitates were su

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Blackwood, Brian P., Douglas R. Wood, Carrie Y. Yuan, et al. "Urinary Claudin-2 Measurements as a Predictor of Necrotizing Enterocolitis: A Pilot Study." Journal of Neonatal Surgery 4, no. 4 (2015): 43. http://dx.doi.org/10.47338/jns.v4.457.

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Background: Necrotizing Enterocolitis (NEC) affects 5-10% of NICU patients where initially patients may have only nonspecific clinical findings. A noninvasive tool for detection would aid in diagnosis. Increased urinary claudins have been associated with active adult inflammatory bowel disease.Methods: Institutional Review Board approval was obtained. Neonatal intestinal tissue samples were obtained from patients with and without NEC. Immunofluorescence analysis of claudin-2 was performed on the intestinal tissue. Thirty two urine samples were collected from 6 NICU patients. Proteins were extr

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Psáder, Roland, Csaba Jakab, Ákos Máthé, Gyula Balka, Kinga Pápa, and Ágnes Sterczer. "Expression of claudins in the normal canine gastric mucosa." Acta Veterinaria Hungarica 62, no. 1 (2014): 13–21. http://dx.doi.org/10.1556/avet.2013.053.

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The aim of the present study was to investigate the expression pattern of claudin-1, -2, -3, -4, -5, -7, -8, -10 and -18 in the intact fundic and pyloric gastric mucosa of dogs. Intense, linear, membranous claudin-18 positivity was detected in the surface gastric cells and in the epithelial cells of the gastric glands both in the fundic and pyloric stomach regions. The mucous neck cells in the apical part of the glands, furthermore the parietal cells and chief cells of the basal part of the gland were all positive for claudin-18, in the same way as the enteroendocrine cells. Cells of the basal

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Paschoud, Serge, Massimo Bongiovanni, Jean-Claude Pache, and Sandra Citi. "Claudin-1 and claudin-5 expression patterns differentiate lung squamous cell carcinomas from adenocarcinomas." Modern Pathology 20, no. 9 (2007): 947–54. http://dx.doi.org/10.1038/modpathol.3800835.

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Oshima, Tadayuki, Hiroto Miwa, and Takashi Joh. "Aspirin induces gastric epithelial barrier dysfunction by activating p38 MAPK via claudin-7." American Journal of Physiology-Cell Physiology 295, no. 3 (2008): C800—C806. http://dx.doi.org/10.1152/ajpcell.00157.2008.

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Tight junctions create a paracellular permeability barrier that is breached when nonsteroidal anti-inflammatory drugs cause gastrointestinal injury, including increased gastrointestinal permeability. However, the mechanism by which aspirin affects the function of gastric epithelial tight junctions is unknown. Thus, we examined the effect of aspirin on gastric mucosal barrier properties and tight junction organization using MKN28, a human gastric epithelial cell line that expresses claudin-3, claudin-4, claudin-7, zonula occludens (ZO)-1, and occludin, but not claudin-2 or claudin-5, as determi

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Sadalla, José Carlos, Sílvia Vanessa Lourenço, Mirian Nacagami Sotto, Edmund Chada Baracat, and Jesus Paula Carvalho. "Claudin and p53 expression in vulvar lichen sclerosus and squamous-cell carcinoma." Journal of Clinical Pathology 64, no. 10 (2011): 853–57. http://dx.doi.org/10.1136/jclinpath-2011-200103.

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AimsVulvar squamous-cell carcinoma (SCC) is a rare gynaecological cancer. Vulvar SCC has been shown to develop from vulvar intraepithelial neoplasias, which are related to lichen sclerosus (LS). Most studies to date have compared vulvar SCC with LS only morphologically, but no detailed molecular analysis has been performed. The objective was to compare claudin and p53 expression in these diseases and determine if there was any association with expression and vulvar SCC progression.MethodsImmunohistochemical analysis was performed in order to determine expression of p53 and claudin 1, 2, 3, 4,

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Fedwick, Jason P., Tamia K. Lapointe, Jonathan B. Meddings, Philip M. Sherman, and Andre G. Buret. "Helicobacter pylori Activates Myosin Light-Chain Kinase To Disrupt Claudin-4 and Claudin-5 and Increase Epithelial Permeability." Infection and Immunity 73, no. 12 (2005): 7844–52. http://dx.doi.org/10.1128/iai.73.12.7844-7852.2005.

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ABSTRACT Helicobacter pylori is a spiral, gram-negative bacterium that specifically and persistently infects the human stomach. In some individuals, H. pylori-induced chronic gastritis may progress to gastroduodenal ulcers and gastric cancer. Currently, the host-microbe interactions that determine the clinical outcome of infection are not well defined. H. pylori strains capable of disrupting the gastric epithelial barrier may increase the likelihood of developing serious disease. In this study, H. pylori strain SS1 increased gastric, but not small intestinal, permeability in C57BL/6 mice. H. p

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Jakab, Csaba, Miklós Rusvai, Péter Gálfi, et al. "Expression of claudin-5 in hepatoid gland biopsies." Veterinary Dermatology 21, no. 3 (2010): 276–81. http://dx.doi.org/10.1111/j.1365-3164.2009.00798.x.

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Mandel, Ilana, Tamar Paperna, Anat Volkowich, Maayan Merhav, Lea Glass-Marmor, and Ariel Miller. "The ubiquitin-proteasome pathway regulates claudin 5 degradation." Journal of Cellular Biochemistry 113, no. 7 (2012): 2415–23. http://dx.doi.org/10.1002/jcb.24118.

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Morita, Kazumasa, Hiroyuki Sasaki, Kyoko Furuse, Mikio Furuse, Shoichiro Tsukita, and Yoshiki Miyachi. "Expression of claudin-5 in dermal vascular endothelia." Experimental Dermatology 12, no. 3 (2003): 289–95. http://dx.doi.org/10.1034/j.1600-0625.2003.120309.x.

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Koda, Ryo, Linning Zhao, Eishin Yaoita, et al. "Novel expression of claudin-5 in glomerular podocytes." Cell and Tissue Research 343, no. 3 (2011): 637–48. http://dx.doi.org/10.1007/s00441-010-1117-y.

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Colamonici, Marco A., Yulia Epshtein, Weiguo Chen, and Jeffrey R. Jacobson. "Haloperidol Attenuates Lung Endothelial Cell Permeability In Vitro and In Vivo." Cells 10, no. 9 (2021): 2186. http://dx.doi.org/10.3390/cells10092186.

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We previously reported that claudin-5, a tight junctional protein, mediates lung vascular permeability in a murine model of acute lung injury (ALI) induced by lipopolysaccharide (LPS). Recently, it has been reported that haloperidol, an antipsychotic medication, dose-dependently increases expression of claudin-5 in vitro and in vivo, in brain endothelium. Notably, claudin-5 is highly expressed in both brain and lung tissues. However, the effects of haloperidol on EC barrier function are unknown. We hypothesized that haloperidol increases lung EC claudin-5 expression and attenuates agonist-indu

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Jacquillet, G., O. Barbier, M. Cougnon, et al. "Zinc protects renal function during cadmium intoxication in the rat." American Journal of Physiology-Renal Physiology 290, no. 1 (2006): F127—F137. http://dx.doi.org/10.1152/ajprenal.00366.2004.

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This study investigates the effect in the rat of chronic CdCl2 intoxication (500 μg Cd2+/kg, daily ip injection for 5 days) on renal function and the changes in tight junction proteins claudin-2, claudin-3, and claudin-5 present in rat kidney. We also studied the effect of coadministration of ZnCl2 (500 μg Zn2+/kg) during chronic CdCl2 intoxication. Our results indicate that 1) most of the filtered Cd2+ is reabsorbed within the kidney; 2) chronic Cd2+ intoxication can induce a change in renal handling of ions without altering glomerular filtration rate; 3) a delayed nephropathy, showing Fancon

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Rossa, Jan, Dorothea Lorenz, Martina Ringling, Anna Veshnyakova, and Joerg Piontek. "Overexpression of claudin-5 but not claudin-3 induces formation of trans-interaction-dependent multilamellar bodies." Annals of the New York Academy of Sciences 1257, no. 1 (2012): 59–66. http://dx.doi.org/10.1111/j.1749-6632.2012.06546.x.

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Jakab, Csaba, Miklós Rusvai, Nóra Biró, Zoltán Szabó, Péter Gálfi, and Janina Kulka. "Claudin-5-positive angioleiomyoma in the uterus of a degu ( Octodon degus )." Acta Veterinaria Hungarica 58, no. 3 (2010): 331–40. http://dx.doi.org/10.1556/avet.58.2010.3.6.

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A 5-year-old female degu ( Octodon degus ) showed the clinical sign of metrorrhagia. During ovariohysterectomy a circumscribed tumoural lesion was found in the right uterine horn. The histopathological diagnosis of this soft tissue mass was primary benign cavernous angioleiomyoma of the uterus. During immunohistochemical analysis the neoplastic endothelial cells of this mixed mesenchymal tumour showed strong membrane positivity for the endothelial marker claudin-5 but were negative for CD31 (another endothelial marker). The endothelial cells of the internal positive control tissues such as int

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Zhang, Jie, Guangming Yang, Yu Zhu, Xiaoyong Peng, Tao Li, and Liangming Liu. "Relationship of Cx43 regulation of vascular permeability to osteopontin-tight junction protein pathway after sepsis in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 1 (2018): R1—R11. http://dx.doi.org/10.1152/ajpregu.00443.2016.

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Our previous study demonstrated that connexin (Cx)43 participated in the regulation of vascular permeability in severe sepsis. Osteopontin (OPN) has been demonstrated to participate in the occurrence of atherosclerosis, inflammation, as well as the adhesion and migration of cells. It is not clear whether OPN is involved in Cx43 regulating vascular permeability after sepsis and if it is related to tight-junction proteins. with the use of cecal ligation and puncture (CLP)-induced septic rats and lipopolysaccharide (LPS)-treated pulmonary vein vascular endothelial cells (VECs), the role of zona o

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Osada, Takashi, Yu-Huan Gu, Masato Kanazawa та ін. "Interendothelial Claudin-5 Expression Depends on Cerebral Endothelial Cell–Matrix Adhesion by β1-Integrins". Journal of Cerebral Blood Flow & Metabolism 31, № 10 (2011): 1972–85. http://dx.doi.org/10.1038/jcbfm.2011.99.

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The hypothesis tested by these studies states that in addition to interendothelial cell tight junction proteins, matrix adhesion by β1-integrin receptors expressed by endothelial cells have an important role in maintaining the cerebral microvessel permeability barrier. Primary brain endothelial cells from C57 BL/6 mice were incubated with β1-rintegrin function-blocking antibody (Ha2/5) or isotype control and the impacts on claudin-5 expression and microvessel permeability were quantified. Both flow cytometry and immunofluorescence studies demonstrated that the interendothelial claudin-5 expres

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Matter, Karl, and Maria S. Balda. "Holey barrier." Journal of Cell Biology 161, no. 3 (2003): 459–60. http://dx.doi.org/10.1083/jcb.200304039.

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Endothelial tight junctions (TJs)**Abbreviations used in this paper: BBB, blood-brain barrier; BEC, brain endothelial cell; TJ, tight junction. are an important functional part of the blood-brain barrier (BBB). In this issue, Nitta et al. (2003) demonstrate that claudin-5, a transmembrane protein of TJs, is a critical determinant of BBB permeability in mice. Unexpectedly, knockout of claudin-5 did not result in a general breakdown of TJs but in a selective increase in paracellular permeability of small molecules. This suggests that the BBB can be manipulated to allow selective diffusion of sma

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Kakogiannos, Nikolaos, Laura Ferrari, Costanza Giampietro та ін. "JAM-A Acts via C/EBP-α to Promote Claudin-5 Expression and Enhance Endothelial Barrier Function". Circulation Research 127, № 8 (2020): 1056–73. http://dx.doi.org/10.1161/circresaha.120.316742.

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Rationale: Intercellular tight junctions are crucial for correct regulation of the endothelial barrier. Their composition and integrity are affected in pathological contexts, such as inflammation and tumor growth. JAM-A (junctional adhesion molecule A) is a transmembrane component of tight junctions with a role in maintenance of endothelial barrier function, although how this is accomplished remains elusive. Objective: We aimed to understand the molecular mechanisms through which JAM-A expression regulates tight junction organization to control endothelial permeability, with potential implicat

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REN, JINGJING, MINGWEI YANG, PENGYAN WANG, JIANJUN JIANG, and GENQIANG YAN. "Specific role of the tight junction proteins occludin and claudin-5 on the blood–brain barrier during Listeria monocytogenes infection." Medycyna Weterynaryjna 76, no. 06 (2020): 6416–2020. http://dx.doi.org/10.21521/mw.6416.

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To investigate the blood-brain barrier (BBB) permeability of mice after Listeria monocytogenes infection for further study on the mechanism of L. monocytogenes crossing the BBB, a mouse model was established and Evans blue assay was performed to assess the BBB disruption. Using relative quantitative real-time PCR, the RNA expression of Zonula occludens-1 (ZO-1), occludin and claudin-5 were detected. In addition, the protein expression level of ZO-1, occludin and claudin-5 were detected by immunohistochemistry and western blot. The extravasation of Evans blue dye was significantly different bet

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Bartosova, Maria, Rebecca Herzog, David Ridinger, et al. "Alanyl-Glutamine Restores Tight Junction Organization after Disruption by a Conventional Peritoneal Dialysis Fluid." Biomolecules 10, no. 8 (2020): 1178. http://dx.doi.org/10.3390/biom10081178.

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Understanding and targeting the molecular basis of peritoneal solute and protein transport is essential to improve peritoneal dialysis (PD) efficacy and patient outcome. Supplementation of PD fluids (PDF) with alanyl-glutamine (AlaGln) increased small solute transport and reduced peritoneal protein loss in a recent clinical trial. Transepithelial resistance and 10 kDa and 70 kDa dextran transport were measured in primary human endothelial cells (HUVEC) exposed to conventional acidic, glucose degradation products (GDP) containing PDF (CPDF) and to low GDP containing PDF (LPDF) with and without

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Lee, Bo Kyung, Soo-Wang Hyun, and Yi-Sook Jung. "Yuzu and Hesperidin Ameliorate Blood-Brain Barrier Disruption during Hypoxia via Antioxidant Activity." Antioxidants 9, no. 9 (2020): 843. http://dx.doi.org/10.3390/antiox9090843.

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Yuzu and its main component, hesperidin (HSP), have several health benefits owing to their anti-inflammatory and antioxidant properties. We examined the effects of yuzu and HSP on blood–brain barrier (BBB) dysfunction during ischemia/hypoxia in an in vivo animal model and an in vitro BBB endothelial cell model, and also investigated the underlying mechanisms. In an in vitro BBB endothelial cell model, BBB permeability was determined by measurement of Evans blue extravasation in vivo and in vitro. The expression of tight junction proteins, such as claudin-5 and zonula occludens-1 (ZO-1), was de

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Burek, Malgorzata, and Carola Y. Förster. "Cloning and characterization of the murine claudin-5 promoter." Molecular and Cellular Endocrinology 298, no. 1-2 (2009): 19–24. http://dx.doi.org/10.1016/j.mce.2008.09.041.

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Sugimoto, Hitoshi, Makoto Nagahara, Yuan Bae, et al. "Clinicopathologic Relevance of Claudin 5 Expression in Breast Cancer." American Journal of Clinical Pathology 143, no. 4 (2015): 540–46. http://dx.doi.org/10.1309/ajcpwgbz6d0oaivj.

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Hess, Rex A., and Carla M. K. Morrow. "Claudin 5, Germ Cells, and the Blood-Testis Barrier." Biology of Reproduction 83, Suppl_1 (2010): 109. http://dx.doi.org/10.1093/biolreprod/83.s1.109.

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