scholarly journals Glucocorticoids Increase VE-Cadherin Expression and Cause Cytoskeletal Rearrangements in Murine Brain Endothelial cEND Cells

2008 ◽  
Vol 28 (6) ◽  
pp. 1139-1149 ◽  
Author(s):  
Kinga G Blecharz ◽  
Detlev Drenckhahn ◽  
Carola Y Förster
Keyword(s):  
Protein Synthesis ◽  
Tight Junction ◽  
Transcriptional Activation ◽  
Adherens Junction ◽  
Barrier Properties ◽  
Positive Influence ◽  
Brain Capillary Endothelial Cell ◽  
Protein Levels ◽  
Junction Protein ◽  
Adherens Junction Proteins

Recent studies have shown the influence of glucocorticoids on the expression of the tight junction protein occludin in the brain capillary endothelial cell line cEND, contributing to improvement in endothelial barrier functions. In this study, we investigated glucocorticoid effects on the expression of the adherens junction proteins VE- (vascular-endothelial) cadherin, α-catenin and β-catenin as well as that of ZO-1, the plaque protein shared by both adherens and tight junctions on stimulation with dexamethasone. We were able to show a positive influence of dexamethasone administration on VE-cadherin protein levels as well as a rearrangement of VE-cadherin protein to the cytoskeleton after dexamethasone treatment. Investigation of transcriptional activation of the VE-cadherin promoter by dexamethasone, however, did not point to direct glucocorticoid-mediated VE-cadherin gene induction but rather suggested indirect steroid effects leading to increased VE-cadherin protein synthesis. Dexamethasone was further shown to induce cellular differentiation into a cobblestone cellular morphology and reinforcement of adherens junctions concomitant with the increased anchorage of VE-cadherin to the actin cytoskeleton. We thus propose that glucocorticoid effects on VE-cadherin protein synthesis and organization are important for the formation of both adherens and tight junction, and for improved barrier properties in microvascular brain endothelial cells.

scholarly journals Protein Level and Infantile Diarrhea in a Postweaning Piglet Model

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Jing Gao ◽  
Jie Yin ◽  
Kang Xu ◽  
Hui Han ◽  
ZeMin Liu ◽  
...  
Keyword(s):  
Tight Junction ◽  
The Other ◽  
Control Group ◽  
Infantile Diarrhea ◽  
Ampk Signaling ◽  
Protein Sources ◽  
Protein Levels ◽  
Junction Protein ◽  
The Relationship ◽  
Postweaning Diarrhea

Infantile diarrhea is a serious public health problem around worldwide and results in millions of deaths each year. The levels and sources of dietary protein are potential sources of diarrhea, but the relationship between the pathogenesis causes of infantile diarrhea and protein intake remains poorly understood. Many studies have indicated that the key to understanding the relationship between the protein in the diet and the postweaning diarrhea of piglets is to explore the influences of protein sources and levels on the mammalian digestion system. The current study was designed to control diarrhea control by choosing different protein levels in the diet and aimed at providing efficient regulatory measures for infantile diarrhea by controlling the protein levels in diets using a postweaning piglets model. To avoid influences from other protein sources, casein was used as the only protein source in this study. Fourteen piglets (7.98±0.14 kg, weaned at 28 d) were randomly allotted to two dietary treatments: a control group (Cont, containing 17% casein) and a high protein group (HP, containing 30% casein). The experiment lasted for two weeks and all animals were free to eat and drink water ad libitum. The diarrhea score (1=normal; 3=watery diarrhea) and growth performance were recorded daily. The results showed that the piglets in HP group had persistent diarrhea during the whole study, while no diarrhea was noticed in the control groups. Also, the feed intake and body weights were reduced in the HP groups compared with the other group (P<0.05). The diarrhea-related mRNA abundances were analyzed by real-time PCR; the results showed that HP treatment markedly decreased the expression of aquaporin (AQP, P<0.05) and the tight junction protein (P<0.05), but increased inflammatory cytokines (P<0.01) than those in control group. In addition, the Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway (P<0.01) was inhibited in the HP group. Intestinal microbiota was tested by 16S sequencing, and we found that the HP group had a low diversity compared the other group. In conclusion, despite being highly digestible, a high casein diet induced postweaning diarrhea and reduced the growth performance of the postweaning piglets. Meanwhile, AQP, tight junction protein, and intestinal immune were compromised. Thus, the mechanism of how a highly digestible protein diet induces diarrhea might be associated with the AMPK signaling pathway and intestinal microbiome.

scholarly journals 137 RIPK4 maintains epidermal barrier integrity by regulating tight junction protein levels

2016 ◽  
Vol 136 (9) ◽  
pp. S184
Author(s):  
G. Tanghe ◽  
C. Urwyler ◽  
P. De Groote ◽  
K. Leurs ◽  
B. Gilbert ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Protein ◽  
Epidermal Barrier ◽  
Barrier Integrity ◽  
Protein Levels ◽  
Junction Protein

scholarly journals Junctional Adhesion Molecule-A Is Critical for the Formation of Pseudocanaliculi and Modulates E-cadherin Expression in Hepatic Cells

2007 ◽  
Vol 282 (38) ◽  
pp. 28137-28148 ◽  
Author(s):  
Genevieve Konopka ◽  
Jackie Tekiela ◽  
Moriah Iverson ◽  
Clive Wells ◽  
Stephen A. Duncan
Keyword(s):  
Tight Junction ◽  
Adhesion Molecule ◽  
Cell Morphology ◽  
Adherens Junction ◽  
Tight Junction Proteins ◽  
Hepatic Cells ◽  
Junction Protein ◽  
Striking Change ◽  
Junction Proteins ◽  
E Cadherin

Hepatocytes are polarized epithelial cells whose function depends upon their ability to distinguish between the apical and basolateral surfaces that are located at intercellular tight junctions. It has been proposed that the signaling cascades originating at these junctions influence cellular activity by controlling gene expression in the cell nucleus. To assess the validity of this proposal with regard to hepatocytes, we depleted expression of the tight junction protein junctional adhesion molecule-A (JAM-A) in the HepG2 human hepatocellular carcinoma cell line. Reduction of JAM-A resulted in a striking change in cell morphology, with cells forming sheets 1-2 cells thick instead of the normal multilayered clusters. In the absence of JAM-A, other tight junction proteins were mislocalized, and pseudocanaliculi, which form the apical face of the hepatocyte, were consequently absent. There was a strong transcriptional induction of the adherens junction protein E-cadherin in cells with reduced levels of JAM-A. This increase in E-cadherin was partially responsible for the observed alterations in cell morphology and mislocalization of tight junction proteins. We therefore propose the existence of a novel mechanism of cross-talk between specific components of tight and adherens junctions that can be utilized to regulate adhesion between hepatic cells.

scholarly journals Supplementation of sodium butyrate protects mice from the development of non-alcoholic steatohepatitis (NASH)

2015 ◽  
Vol 114 (11) ◽  
pp. 1745-1755 ◽  
Author(s):  
Cheng Jun Jin ◽  
Cathrin Sellmann ◽  
Anna Janina Engstler ◽  
Doreen Ziegenhardt ◽  
Ina Bergheim
Keyword(s):  
Body Weight ◽  
Tight Junction ◽  
Liver Damage ◽  
Sodium Butyrate ◽  
The Body ◽  
Tight Junction Protein ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Alcoholic Steatohepatitis ◽  
Junction Protein

AbstractOvernutrition, insulin resistance and an impaired intestinal barrier function are discussed as critical factors in the development of non-alcoholic fatty liver disease. Not only butyrate-producing probiotics as well as supplementation of sodium butyrate (SoB) have been suggested to bear protective effects on liver damage of various aetiologies. However, whether an oral consumption of SoB has a protective effect on Western-style diet (WSD)-induced non-alcoholic steatohepatitis (NASH) and if so molecular mechanism involved has not yet been determined. Eight-week-old C57BL/6J mice were pair-fed either a liquid control or WSD±0·6 g/kg body weight SoB. After 6 weeks, markers of liver damage, inflammation, toll-like receptor (TLR)-4 signalling, lipid peroxidation and glucose as well as lipid metabolism were determined in the liver tissue. Tight junction protein levels were determined in the duodenal tissue. SoB supplementation had no effects on the body weight gain or liver weight of WSD-fed mice, whereas liver steatosis and hepatic inflammation were significantly decreased (e.g. less inflammatory foci and neutrophils) when compared with mice fed only a WSD. Tight junction protein levels in duodenum, hepatic mRNA expression of TLR-4 and sterol regulatory element-binding protein 1c were altered similarly in both WSD groups when compared with controls, whereas protein levels of myeloid differentiation primary response gene 88, inducible nitric oxide synthase, 4-hydroxynonenal protein adducts and F4/80 macrophages were only significantly induced in livers of mice fed only the WSD. In summary, these data suggest that an oral supplementation of SoB protects mice from inflammation in the liver and thus from the development of WSD-induced NASH.

Regulation of Adherens Junction Protein Levels: Its Role in Cell Motility and Tumorigenicity

1995 ◽  
pp. 143-163 ◽  
Author(s):  
Avri Ben-Zéev ◽  
José Luis Rodriguez Fernández ◽  
Ursula Glück ◽  
Daniela Salomon ◽  
Margot Zöller ◽  
...  
Keyword(s):  
Cell Motility ◽  
Adherens Junction ◽  
Protein Levels ◽  
Adherens Junction Protein ◽  
Junction Protein

scholarly journals Modulations of genes related to gut integrity, apoptosis, and immunity underlie the beneficial effects of Bacillus amyloliquefaciens CECT 5940 in broilers fed diets with different protein levels in a necrotic enteritis challenge model

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Kosar Gharib-Naseri ◽  
Juliano Cesar de Paula Dorigam ◽  
Kiran Doranalli ◽  
Sarbast Kheravii ◽  
Robert A. Swick ◽  
...  
Keyword(s):  
Tight Junction ◽  
Protein Level ◽  
Bacillus Amyloliquefaciens ◽  
Crude Protein ◽  
Immunoglobulin M ◽  
Mucosal Barrier ◽  
Necrotic Enteritis ◽  
Protein Levels ◽  
Junction Protein ◽  
Crude Protein Level

Abstract Background The ban of in-feed antimicrobial additives has negatively affected the poultry industry by causing necrotic enteritis (NE) to emerge in the flocks. Alternatives such as Bacillus probiotics have shown to be effective on eliminating the negative effects of this disease. Two experiments were conducted to investigate the effect of Bacillus amyloliquefaciens CECT 5940 (BA) in broiler chickens under NE challenge and/or fed diets with different protein levels. Methods In both experiments, 480 day-old mix-sexed Ross-308 broilers were arranged in a 2 × 2 factorial arrangement of treatments. In experiment 1, the factors were NE challenge (yes or no) and probiotic (yes or no). In experiment 2, the factors were dietary crude protein levels (standard or reduced) and probiotic (yes or no) and were used under NE challenge condition. Oral administration of Eimeria oocysts (day 9) followed by inoculation with Clostridium perfringens (day 14 and 15) was used to induce NE challenge. On day 16, two birds from each treatment were gavaged with fluorescein isothiocyanate-dextran (FITC-d) and blood samples were collected for gut integrity evaluation, and jejunal samples were collected for gene expression assay. Results In experiment 1, BA supplementation decreased caspase-3 (CASP3) (P < 0.001) and caspase-8 (CASP8) (P < 0.05) and increased occludin (OCLD) (P < 0.05) expression regardless of the challenge. Additionally, BA supplementation downregulated interfron-γ (IFN-γ) expression (P < 0.01) and upregulated immunoglobulin-G (IgG) (P < 0.01) and immunoglobulin-M (IgM) (P < 0.05) only in challenged birds. In experiment 2, the expression of genes encoding mucin-2 (MUC2) (P < 0.001), tight junction protein-1 (TJP1) (P < 0.05) and OCLD (P < 0.05) were upregulated by the addition of BA in the diet, regardless of the crude protein level. Further, BA supplementation downregulated INF-γ (P < 0.01) and upregulated immunoglobulin-A (IgA) (P < 0.05), IgM (P < 0.05) and IgG (P < 0.01) regardless of the crude protein level. Conclusion These findings suggest that supplementation of BA in broiler diets can improve gut health by modulation of genes related to the mucosal barrier, tight junction, and immunity in broilers challenged by unfavourable conditions such as NE challenge.

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