Hyaluronan 35 kDa treatment protects mice from Citrobacter rodentium infection and induces epithelial tight junction protein ZO-1 in vivo

This study aimed to assess the effect of gonadotrophin suppression and FSH replacement on testicular tight junction dynamics and blood–testis barrier (BTB) organisation in vivo, utilising the seasonal breeding Djungarian hamster. Confocal immunohistology was used to assess the cellular organisation of tight junction proteins and real-time PCR to quantify tight junction mRNA. The effect of tight junction protein organisation on the BTB permeability was also investigated using a biotin-linked tracer. Tight junction protein (claudin-3, junctional adhesion molecule (JAM)-A and occludin) localisation was present but disorganised after gonadotrophin suppression, while mRNA levels (claudin-11, claudin-3 and occludin) were significantly (two- to threefold) increased. By contrast, both protein localisation and mRNA levels for the adaptor protein zona occludens-1 decreased after gonadotrophin suppression. FSH replacement induced a rapid reorganisation of tight junction protein localisation. The functionality of the BTB (as inferred by biotin tracer permeation) was found to be strongly associated with the organisation and localisation of claudin-11. Surprisingly, JAM-A was also recognised on spermatogonia, suggesting an additional novel role for this protein in trans-epithelial migration of germ cells across the BTB. It is concluded that gonadotrophin regulation of tight junction proteins forming the BTB occurs primarily at the level of protein organisation and not gene transcription in this species, and that immunolocalisation of the organised tight junction protein claudin-11 correlates with BTB functionality.

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Tight junction protein claudin-6 inhibits growth and induces the apoptosis of cervical carcinoma cells in vitro and in vivo

Medical Oncology ◽

10.1007/s12032-015-0600-4 ◽

2015 ◽

Vol 32 (5) ◽

Cited By ~ 14

Author(s):

Xiaowei Zhang ◽

Yang Ruan ◽

Yanru Li ◽

Dongjing Lin ◽

Chengshi Quan

Keyword(s):

Tight Junction ◽

Cervical Carcinoma ◽

Carcinoma Cells ◽

Tight Junction Protein ◽

Junction Protein

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Correlation of occludin protein mobility with paracellular leak pathway permeability in renal epithelia

10.1101/437996 ◽

2018 ◽

Author(s):

Josephine Axis ◽

Alexander L. Kolb ◽

Robert L. Bacallao ◽

Kurt Amsler

Keyword(s):

Tight Junction ◽

Ischemia Reperfusion Injury ◽

Mdck Cells ◽

Ischemia Reperfusion ◽

Paracellular Permeability ◽

Tight Junction Protein ◽

Protein Mobility ◽

Junction Protein ◽

Leak Pathway

ABSTRACTStudies have demonstrated regulation of the epithelial paracellular permeability barrier, the tight junction, by a variety of stimuli. Recent studies have reported a correlation between changes in paracellular permeability, particularly paracellular permeability to large solutes (leak pathway), and mobility of the tight junction protein, occludin, in the plane of the plasma membrane. This had led to the hypothesis that changes in occludin protein mobility are causative for changes in paracellular permeability. Using a renal epithelial cell model system, MDCK, we examined the effect of various manipulations on both leak pathway permeability, monitored as the paracellular movement of a fluorescent molecule (calcein), and occludin protein mobility, monitored through fluorescence recovery after photobleaching. Our results indicate that knockdown of the associated tight junction protein, ZO-1, increases baseline leak pathway permeability, whereas, knockdown of the related tight junction protein, ZO-2, does not alter baseline leak pathway permeability. Knockdown of either ZO-1 or ZO-2 decreases the rate of movement of occludin protein but only knockdown of ZO-2 protein alters the percent of occludin protein that is mobile. Further, treatment with hydrogen peroxide increases leak pathway permeability in wild type MDCK cells and in ZO-2 knockdown MDCK cells but not in ZO-1 knockdown MDCK cells. This treatment decreases the rate of occludin movement in all three cell lines but only alters the mobile fraction of occludin protein in ZO-1 knockdown MDCK cells. Finally, we examined the effect of renal ischemia/reperfusion injury on occludin protein mobility in vivo.Ischemia/reperfusion injury both increased the rate of occludin mobility and increased the fraction of occludin protein that is mobile. These results indicate that, at least in our cell culture and in vivo model systems, there is no consistent correlation between paracellular leak pathway permeability and occludin protein mobility.

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Su1945 Histone Deacetylases Regulate Epithelial Tight Junction Protein Expression and Prevent Chronic Stress-induced Visceral Hyperalgesia

Gastroenterology ◽

10.1016/s0016-5085(16)32044-3 ◽

2016 ◽

Vol 150 (4) ◽

pp. S596

Author(s):

Ye Zong ◽

Shuangsong Hong ◽

John W. Wiley

Keyword(s):

Protein Expression ◽

Tight Junction ◽

Chronic Stress ◽

Histone Deacetylases ◽

Tight Junction Protein ◽

Visceral Hyperalgesia ◽

Tight Junction Protein Expression ◽

Junction Protein ◽

Epithelial Tight Junction

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Lnc-ECAL-1 controls cerebrovascular homeostasis by targeting endothelium-specific tight junction protein Cldn5b

10.1101/2020.01.30.926279 ◽

2020 ◽

Author(s):

Fang-Fang Li ◽

Yu-Lai Liang ◽

Jing-Jing Zhang ◽

Qing Jing

Keyword(s):

Tight Junction ◽

Intracranial Hemorrhage ◽

Network Formation ◽

Bioinformatic Analysis ◽

Cerebrovascular Diseases ◽

Confocal Imaging ◽

Tight Junction Protein ◽

Junction Protein ◽

Attractive Therapeutic Target

AbstractCerebrovascular disorder-induced brain blood flow interruption or intracranial hemorrhage pose a great threaten to health. Emerging roles of long-noncoding RNAs (lncRNAs) in diagnosis and treatment of cardiovascular diseases have been recognized. However, whether and how lncRNAs modulate vascular homeostasis, especially network formation remain largely unknown. Here, we identified ECAL-1, a long non-coding RNA, as an important determinant for cerebrovascular homeostasis. Using the morpholino- and CRISPR /Cas9-based genetic modifications in combination with in vivo confocal imaging in zebrafish, we claimed that inactivation of ECAL-1 induced the apparent distortion of cerebral vascular pattern accompanied by intracranial hemorrhage. These cerebrovascular abnormalities were associated with decreased proliferation and anomalous interconnection of endothelial cells. Importantly, overexpression of Cldn5b, an endothelial cell-specific tight junction protein-encoding gene, could partially rescued the phenotype induced by ECAL-1 deficiency. Furthermore, bioinformatic analysis and experimental validation revealed that ECAL-1 sponged miR-23a, which targeted Cldn5b 3’UTR and modulated Cldn5b expression, to maintain cerebrovascular pattern formation and integrity. Our results presented here revealed that ECAL-1 specifically controls cerebrovascular network formation and integrity through targeting miR-23a-Cldn5b axis. These findings provide a new regulation modality for cerebrovascular patterning and the potential neurovascular disorders, and ECAL-1-miR-23a axis represents as an attractive therapeutic target for cerebrovascular diseases.

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