Claudins: Control of Barrier Function and Regulation in Response to Oxidant Stress

Overgaard, Christian E.; Daugherty, Brandy L.; Mitchell, Leslie A.; Koval, Michael

doi:10.1089/ars.2011.3893

Cited by 98 publications

(88 citation statements)

References 148 publications

(155 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Consistently, as an activator of MMP-9, MMP-3 reduction in malignant gliomas was induced by inactivated NF-κB [26]. Claudins are members of the class of proteins involved in tight junctions [27]. Cldn1 and Cldn4 expression has been detected in many cancers, including ovarian cancer and esophageal cancer [28,29].…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 94%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Numerous studies have highlighted the activation of NF-κB in the esophageal mucosa during the early stages of gastroesophageal reflux disease (GERD). The present study aimed to investigate the role of the TLR4/NF-κB signaling pathway in GERD rat models. Methods: Wistar rats (n = 60) were recruited to establish a GERD animal model. Distal esophageal pH was assessed, followed by determination of the contents of thiobarbituric acid-reactive species (TBARS) and reactive oxygen species (ROS) in esophageal mucosa homogenate. ELISA was employed to detect the levels of inflammatory factors (IL-6, IL-8, IL-10 and TNF-α) in esophageal mucosa. The expression of MMP-3, MPP-9, Cldn1 and Cldn4 was determined by immunohistochemistry. RT-qPCR and western blot analysis were applied to evaluate the protein expressions in TLR4/NF-κB signaling pathway, while TUNEL staining was utilized to examine the apoptosis rate in the esophageal mucosal tissues. Results: Distal esophageal pH of the rats was higher in the GERD + PDTC group than in other groups. Levels of inflammatory factors in esophageal mucosal tissues were downregulated with the inhibition of NF-κB, which was determined to be associated with the decreased contents of TBARS and ROS. Moreover, decreased MMP-3 and MPP-9 in addition to elevated Cldn1 and Cldn4 were detected in the esophageal mucosa as a result of the inactivation of NF-κB. The TLR4/NF-κB signaling pathway-related proteins (TLR4, NF-κB and IκBα); the rate of apoptosis was demonstrated to be suppressed in the GERD + PDTC group, while inactivating NF-κB was found to alleviate the tissue damage observed in the esophageal mucosa. Conclusion: The key findings of the current study demonstrate that the inactivation of the TLR4/NF-κB signaling pathway alleviates oxidative stress injury and promotes the repair of esophageal mucosal injury among rats with GERD, highlighting a potential novel GERD mechanism.

show abstract

Section: Cellular Physiology and Biochemistrymentioning

confidence: 94%

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Yu¹,

Wang²,

Zhang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Similar to occludin, the PDZ domain in the c-terminus of claudin interacts with ZO-1 and connects claudins with actin cytoskeleton. The composition of claudins varies in different endothelial barriers and, hence, determines whether the barrier is selectively permeable (e.g., the ion selective pores in the kidney) or impermeable (e.g., blood-brain barrier) (328). Pore-forming claudins such as claudin 2 (Cldn-2) form pores that are specific to monovalent cations and water and are found in Madin-Darby Canine Kidney (MDCK) cells.…”

Section: A Tight Junctionsmentioning

confidence: 99%

“…Pore-forming claudins such as claudin 2 (Cldn-2) form pores that are specific to monovalent cations and water and are found in Madin-Darby Canine Kidney (MDCK) cells. The claudins involved in the sealing of TJs include claudin 1, 3, 5, 11, and 19 (328). Of these claudins, claudin 5 is highly expressed in the blood-brain barrier, and claludin 5 -/ -null mice die within 10 h after birth (320).…”

Section: A Tight Junctionsmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,620

2,424

View full text Add to dashboard Cite

Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

show abstract

“…For example, whereas claudin-4 levels are associated with intact alveolar barrier function (199), elevated levels of the highly homologous protein claudin-3 increase paracellular permeability of the alveolar epithelium (161). Tight junction proteins are targets of oxidative stress and, thus, stimuli that lead to redox imbalance with ROS overproduction, since pathogens, inflammatory mediators, hypoxia, hyperoxia, noxious gases, alcohol, or cigarette smoke may alter alveolarcapillary barrier function, thereby contributing to ALI (26,177,179). Similarly to the epithelium, endothelial tight and adherens junctions are also targets of pathological stimuli during ALI (210,225,241) (Fig.…”

Section: L669 Acute Lung Injury and Barrier Dysfunctionmentioning

confidence: 99%

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Herold

Gabrielli

Vadász

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

183

178

View full text Add to dashboard Cite

Herold S, Gabrielli NM, Vadász I. Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction. Am J Physiol Lung Cell Mol Physiol 305: L665-L681, 2013. First published September 13, 2013 doi:10.1152/ajplung.00232.2013In this review we summarize recent major advances in our understanding on the molecular mechanisms, mediators, and biomarkers of acute lung injury (ALI) and alveolar-capillary barrier dysfunction, highlighting the role of immune cells, inflammatory and noninflammatory signaling events, mechanical noxae, and the affected cellular and molecular entities and functions. Furthermore, we address novel aspects of resolution and repair of ALI, as well as putative candidates for treatment of ALI, including pharmacological and cellular therapeutic means. alveolar-capillary barrier dysfunction; molecular mechanism; pharmacological and cell-based therapy; pulmonary edema; zaacute lung injury/acute respiratory distress syndrome Immune Cells and Inflammatory Signaling Pathways in ALIOne of the central concepts in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is that an unbalanced quantity or quality of the inflammatory response aggravates epithelial or endothelial injury. This includes a dysregulated recruitment of leukocytes and/or an exaggerated activation of these cells; inappropriate expression of cytokines, lipid mediators, or reactive oxygen species; enhanced activation of death receptor signaling (97,98,140,207,240); or an uncontrolled activity of platelets or the coagulation cascade (154). In general, these responses are initiated and maintained by recognition of danger-or pathogen-associated molecular patterns

show abstract

Claudins: Control of Barrier Function and Regulation in Response to Oxidant Stress

Cited by 98 publications

References 148 publications

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Involvement of the TLR4/NF-κB Signaling Pathway in the Repair of Esophageal Mucosa Injury in Rats with Gastroesophageal Reflux Disease

Reactive Oxygen Species in Inflammation and Tissue Injury

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Contact Info

Product

Resources

About