scholarly journals The transmembrane protein Macroglobulin complement-related is essential for septate junction formation and epithelial barrier function in Drosophila

Development ◽  
2014 ◽  
Vol 141 (4) ◽  
pp. 899-908 ◽  
Author(s):  
T. Batz ◽  
D. Forster ◽  
S. Luschnig
Keyword(s):  
Barrier Function ◽  
Transmembrane Protein ◽  
Septate Junction ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Junction Formation

scholarly journals Thermal acclimation mitigates cold-induced paracellular leak from the Drosophila gut

2017 ◽  
Author(s):  
Heath A. MacMillan ◽  
Gil Yerushalmi ◽  
Sima Jonusaite ◽  
Scott P. Kelly ◽  
Andrew Donini
Keyword(s):  
Cold Acclimation ◽  
Barrier Function ◽  
Chilling Injury ◽  
Septate Junction ◽  
Epithelial Barrier ◽  
Concentration Gradients ◽  
Epithelial Barrier Function ◽  
Occluding Junctions ◽  
Composition And Structure ◽  
Summary Statement

AbstractWhen chilled to temperatures below their critical thermal minimum, chill susceptible insects can suffer tissue damage and die. The mechanisms that cause this chilling injury are not well understood but a growing body of evidence suggests that a loss of ion and water homeostasis in the cold leads to hemolymph hyperkalemia that depolarizes cells, leading to cell death. The apparent root of this cascade of issues is the net leak of osmolytes down their concentration gradients in the cold. Many insects, however, are capable of adjusting their thermal physiology, and cold-acclimated Drosophila can maintain homeostasis and avoid chilling injury better than warm-acclimated flies. Here, we test whether the cold-induced loss of osmotic homeostasis is associated with a loss of epithelial barrier function in Drosophila, and provide the first evidence of cold-induced epithelial barrier failure in an invertebrate. Flies exposed to 0° C had increased rates of paracellular leak through the gut epithelia, but cold acclimation reduced paracellular permeability, both before and during cold stress, and improved cold tolerance. This adjustment in barrier function was associated with changes in the abundance of select septate junction proteins and the appearance of a tortuous ultrastructure in subapical intercellular regions of contact between adjacent midgut epithelial cells. Thus, cold causes paracellular leak in a chill susceptible insect and cold acclimation can mitigate this effect, at least partly through changes in the composition and structure of transepithelial barriers.Summary Statement:Chilling disrupts barrier function of the gut of flies and cold acclimation can mitigate this problem through changes in paracellular occluding junctions.

scholarly journals The septate junction protein Snakeskin is critical for epithelial barrier function and tissue homeostasis in the Malpighian tubules of adult Drosophila

2020 ◽  
Author(s):  
Anthony J Dornan ◽  
Kenneth A Halberg ◽  
Liesa-Kristin Beuter ◽  
Shireen-Anne Davies ◽  
Julian A.T. Dow
Keyword(s):  
Barrier Function ◽  
Tissue Homeostasis ◽  
Malpighian Tubules ◽  
Septate Junction ◽  
Epithelial Barrier ◽  
Renal Tubules ◽  
Epithelial Barrier Function ◽  
Adhesion Protein ◽  
Junction Protein ◽  
Secretory Transport

Transporting epithelia provide a protective physical barrier while directing appropriate transport of ions, solutes and water. In invertebrates, epithelial integrity is dependent on formation, and maintenance, of ′tight′ septate junctions (SJs). We demonstrated that Drosophila Malpighian (renal) tubules undergo an age-dependent decline in secretory transport capacity, which correlates with mislocalisation of SJ proteins and coincident progressive degeneration in cellular morphology and tissue homeostasis. By restrictively impairing, in adult tubules, the cell adhesion protein Snakeskin, which is essential for smooth SJ formation, we observed progressive changes in cellular and tissue morphology that phenocopied these effects, including mislocalisation of junctional proteins with concomitant loss of cell polarity and barrier function. Resulting in significant accelerated decline in tubule secretory capacity and organismal viability. Our investigations highlight the tubule′s essential role in maintenance of organismal health, while providing measurable markers of compromised epithelial barrier and tissue function that manifest in advanced morbidity and death.

scholarly journals PGC-1α mediates a metabolic host defense response in human airway epithelium during rhinovirus infections

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Aubrey N. Michi ◽  
Bryan G. Yipp ◽  
Antoine Dufour ◽  
Fernando Lopes ◽  
David Proud
Keyword(s):  
Host Defense ◽  
Barrier Function ◽  
Bacterial Infections ◽  
Molecular Mechanisms ◽  
Cellular Damage ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
Epithelial Damage

AbstractHuman rhinoviruses (HRV) are common cold viruses associated with exacerbations of lower airways diseases. Although viral induced epithelial damage mediates inflammation, the molecular mechanisms responsible for airway epithelial damage and dysfunction remain undefined. Using experimental HRV infection studies in highly differentiated human bronchial epithelial cells grown at air-liquid interface (ALI), we examine the links between viral host defense, cellular metabolism, and epithelial barrier function. We observe that early HRV-C15 infection induces a transitory barrier-protective metabolic state characterized by glycolysis that ultimately becomes exhausted as the infection progresses and leads to cellular damage. Pharmacological promotion of glycolysis induces ROS-dependent upregulation of the mitochondrial metabolic regulator, peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), thereby restoring epithelial barrier function, improving viral defense, and attenuating disease pathology. Therefore, PGC-1α regulates a metabolic pathway essential to host defense that can be therapeutically targeted to rescue airway epithelial barrier dysfunction and potentially prevent severe respiratory complications or secondary bacterial infections.

The enteric nervous system as a regulator of intestinal epithelial barrier function in health and disease

2010 ◽  
Vol 4 (5) ◽  
pp. 637-651 ◽  
Author(s):  
Susanne A Snoek ◽  
Marleen I Verstege ◽  
Guy E Boeckxstaens ◽  
René M van den Wijngaard ◽  
Wouter J de Jonge
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Health And Disease

scholarly journals JunD Represses Transcription and Translation of the Tight Junction Protein Zona Occludens-1 Modulating Intestinal Epithelial Barrier Function

2008 ◽  
Vol 19 (9) ◽  
pp. 3701-3712 ◽  
Author(s):  
Jie Chen ◽  
Lan Xiao ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Mrna Translation ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function

The AP-1 transcription factor JunD is highly expressed in intestinal epithelial cells, but its exact role in maintaining the integrity of intestinal epithelial barrier remains unknown. The tight junction (TJ) protein zonula occludens (ZO)-1 links the intracellular domain of TJ-transmembrane proteins occludin, claudins, and junctional adhesion molecules to many cytoplasmic proteins and the actin cytoskeleton and is crucial for assembly of the TJ complex. Here, we show that JunD negatively regulates expression of ZO-1 and is implicated in the regulation of intestinal epithelial barrier function. Increased JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed ZO-1 expression and increased epithelial paracellular permeability. JunD regulated ZO-1 expression at the levels of transcription and translation. Transcriptional repression of ZO-1 by JunD was mediated through cAMP response element-binding protein-binding site within its proximal region of the ZO-1-promoter, whereas induced JunD inhibited ZO-1 mRNA translation by enhancing the interaction of the ZO-1 3′-untranslated region with RNA-binding protein T cell-restricted intracellular antigen 1-related protein. These results indicate that JunD is a biological suppressor of ZO-1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function.

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