scholarly journals Desmoglein-4 Deficiency Exacerbates Psoriasiform Dermatitis in Rats While Psoriasis Patients Displayed a Decreased Gene Expression of DSG4

2021 ◽  
Vol 12 ◽  
Author(s):  
Tamara Moreno-Sosa ◽  
María Belén Sánchez ◽  
Elisa Olivia Pietrobon ◽  
Juan Manuel Fernandez-Muñoz ◽  
Felipe Carlos Martín Zoppino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skin Diseases ◽  
Skin Inflammation ◽  
Sprague Dawley ◽  
Immune Mediated ◽  
Healthy Cohort ◽  
Underlying Mechanisms ◽  
New Biomarkers ◽  
Inflammatory Changes ◽  
The Impact

Desmogleins are involved in cell adhesion conferring structural skin integrity. However, their role in inflammation has been barely studied, and whether desmoglein-4 modulates psoriasis lesions is completely unknown. In this study, we assessed the impact of desmoglein-4 deficiency on the severity of imiquimod (IMQ)-induced skin inflammation and psoriasiform lesions. To this end, desmoglein-4−/− Oncins France Colony A (OFA) with Sprague–Dawley (SD) genetic background were used. Additionally, human RNA-Seq datasets from psoriasis (PSO), atopic dermatitis (AD), and a healthy cohort were analyzed to obtain a desmosome gene expression overview. OFA rats displayed an intense skin inflammation while SD showed only mild inflammatory changes after IMQ treatment. We found that IMQ treatment increased CD3+ T cells in skin from both OFA and SD, being higher in desmoglein-4-deficient rats. In-depth transcriptomic analysis determined that PSO displayed twofold less DSG4 expression than healthy samples while both, PSO and AD showed more than three-fold change expression of DSG3 and DSC2 genes. Although underlying mechanisms are still unknown, these results suggest that the lack of desmoglein-4 may contribute to immune-mediated skin disease progression, promoting leukocyte recruitment to skin. Although further research is needed, targeting desmoglein-4 could have a potential impact on designing new biomarkers for skin diseases.

Molecular Targets of Phytochemicals for Skin Inflammation

2018 ◽  
Vol 24 (14) ◽  
pp. 1533-1550 ◽  
Author(s):  
Jong-Eun Kim ◽  
Ki Won Lee
Keyword(s):  
Skin Diseases ◽  
Molecular Targets ◽  
Skin Inflammation ◽  
Mechanisms Of Action ◽  
The Body ◽  
Cellular Damage ◽  
Aesthetic Appearance ◽  
Immune Mediated ◽  
Skin Conditions ◽  
Effects Of Aging

Skin is a protective organ and the largest of the human body. Due to its pivotal role in aesthetic appearance, skin health has a significant impact on quality of life. Chronic inflammation of the skin often marks the beginning of various skin diseases. Immune-mediated responses serve to protect the body from external insults and require succinct control, and can lead to ongoing cellular damage and various skin conditions if left unchecked. Studies have shown that phytochemicals can alter processes involved in skin inflammation and alleviate the effects of aging, cancer, atopic dermatitis, psoriasis, and vitiligo. Direct molecular targets of some phytochemicals have been identified and their precise mechanisms of action investigated. In this review, we summarize recent findings on the effects of phytochemicals on skin inflammation and the mechanisms of action involved.

scholarly journals Carbohydrate-Responsive Gene Expression in the Adipose Tissue of Rats

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 153-164 ◽  
Author(s):  
Kartik Shankar ◽  
Amanda Harrell ◽  
Ping Kang ◽  
Rohit Singhal ◽  
Martin J. J. Ronis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Body Weight ◽  
Adipose Tissue ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Oral Glucose ◽  
Sprague Dawley ◽  
Simple Carbohydrates ◽  
The Impact

Abstract Although obesity is often associated with high-fat diets, it can develop from a variety of meal patterns. Excessive intake of simple carbohydrates is one consistent eating behavior leading to obesity. However, the impact of overconsumption of diets with high carbohydrate to fat ratios (C/F) on body composition and global adipose tissue gene expression remains unclear. We used total enteral nutrition to evaluate the effects of caloric intake and C/F on body weight gain and development of obesity. Female Sprague Dawley rats were fed diets with either low C/F or high C/F (HC) (reflecting a 19.5-fold increase in C/F) at two levels of caloric intake: 187 or 220 kcal/kg3/4 · d (15% excess) for 4 wk. At the end of the study period, rats fed HC diets had about 20% higher body weight at either caloric intake compared with rats fed low C/F diets (P < 0.05). Body composition (assessed by nuclear magnetic resonance, computerized tomography, and adipose tissue weights) revealed higher percent fat mass (P < 0.05) in HC rats. Obesity was associated with increased serum resistin, leptin, fasting hyperinsulinemia, and insulin resistance after an oral glucose challenge (P < 0.05). Microarray analyses of adipose tissues revealed HC diets led to changes in 270 and 464 transcripts at 187 and 220 kcal/kg3/4 · d intakes. Genes regulating glucose transport, glycolysis, fatty acid and triglyceride biosynthesis, desaturation and elongation, adipogenesis, and adipokines were affected by HC diets. These results suggest that C/F and interactions with excessive caloric intake per se may regulate body composition and play important roles in the development of obesity and metabolic syndrome.

scholarly journals NF-κB inhibition in keratinocytes causes RIPK1-mediated necroptosis and skin inflammation

2021 ◽  
Vol 4 (6) ◽  
pp. e202000956
Author(s):  
Snehlata Kumari ◽  
Trieu-My Van ◽  
Daniela Preukschat ◽  
Hannah Schuenke ◽  
Marijana Basic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Tumor Necrosis ◽  
Kinase Activity ◽  
Tumor Necrosis Factor Receptor ◽  
Skin Inflammation ◽  
Interacting Protein ◽  
Inflammatory Gene Expression ◽  
Underlying Mechanisms ◽  
Necrosis Factor

Tumor necrosis factor receptor 1 (TNFR1) activates NF-κB–dependent pro-inflammatory gene expression, but also induces cell death by triggering apoptosis and necroptosis. Inhibition of inhibitor of NF-κB kinase (IKK)/NF-κB signaling in keratinocytes paradoxically unleashed spontaneous TNFR1-mediated skin inflammation in mice, but the underlying mechanisms remain poorly understood. Here, we show that TNFR1 causes skin inflammation in mice with epidermis-specific knockout of IKK2 by inducing receptor interacting protein kinase 1 (RIPK1)–dependent necroptosis, and to a lesser extent also apoptosis, of keratinocytes. Combined epidermis-specific ablation of the NF-κB subunits RelA and c-Rel also caused skin inflammation by inducing TNFR1-mediated keratinocyte necroptosis. Contrary to the currently established model that inhibition of NF-κB–dependent gene transcription causes RIPK1-independent cell death, keratinocyte necroptosis, and skin inflammation in mice with epidermis-specific RelA and c-Rel deficiency also depended on RIPK1 kinase activity. These results advance our understanding of the mechanisms regulating TNFR1-induced cell death and identify RIPK1-mediated necroptosis as a potent driver of skin inflammation.

scholarly journals Microbiota and Immune-Mediated Skin Diseases—An Overview

2019 ◽  
Vol 7 (9) ◽  
pp. 279 ◽  
Author(s):  
Adrian Catinean ◽  
Maria Adriana Neag ◽  
Andrei Otto Mitre ◽  
Corina Ioana Bocsan ◽  
Anca Dana Buzoianu
Keyword(s):  
Autoimmune Diseases ◽  
Beneficial Effect ◽  
Skin Diseases ◽  
Experimental Studies ◽  
Immune Mediated ◽  
The Impact ◽  
The Relationship

In recent years, increased attention has been paid to the relationship between microbiota and various diseases, especially immune-mediated diseases. Because conventional therapy for many autoimmune diseases is limited both in efficacy and safety, there is an increased interest in identifying nutraceuticals, particularly probiotics, able to modulate the microbiota and ameliorate these diseases. In this review, we analyzed the research focused on the role of gut microbiota and skin in immunity, their role in immune-mediated skin diseases (IMSDs), and the beneficial effect of probiotics in patients with this pathology. We selected articles published between 2009 and 2019 in PubMed and ScienceDirect that provided information regarding microbiota, IMSDs and the role of probiotics in these diseases. We included results from different types of studies including observational and interventional clinical trials or in vivo and in vitro experimental studies. Our results showed that probiotics have a beneficial effect in changing the microbiota of patients with IMSDs; they also influence disease progression. Further studies are needed to better understand the impact of new therapies on intestinal microbiota. It is also important to determine whether the microbiota of patients with autoimmune diseases can be manipulated in order to restore homeostasis of the microbiota.

scholarly journals Probiotics Modulate Mouse Gut Microbiota and Influence Intestinal Immune and Serotonergic Gene Expression in a Site-Specific Fashion

2021 ◽  
Vol 12 ◽  
Author(s):  
Valentina Taverniti ◽  
Valentina Cesari ◽  
Giorgio Gargari ◽  
Umberto Rossi ◽  
Cristina Biddau ◽  
...  
Keyword(s):  
Gene Expression ◽  
Intestinal Microbiota ◽  
Bifidobacterium Bifidum ◽  
Lactobacillus Helveticus ◽  
Bacterial Strains ◽  
Main Gene ◽  
Underlying Mechanisms ◽  
A Site ◽  
The Impact

Probiotic microorganisms may benefit the host by influencing diverse physiological processes, whose nature and underlying mechanisms are still largely unexplored. Animal models are a unique tool to understand the complexity of the interactions between probiotic microorganisms, the intestinal microbiota, and the host. In this regard, in this pilot study, we compared the effects of 5-day administration of three different probiotic bacterial strains (Bifidobacterium bifidum MIMBb23sg, Lactobacillus helveticus MIMLh5, and Lacticaseibacillus paracasei DG) on three distinct murine intestinal sites (ileum, cecum, and colon). All probiotics preferentially colonized the cecum and colon. In addition, probiotics reduced in the ileum and increased in the cecum and colon the relative abundance of numerous bacterial taxonomic units. MIMBb23sg and DG increased the inducible nitric oxide synthase (iNOS) in the ileum, which is involved in epithelial homeostasis. In addition, MIMBb23sg upregulated cytokine IL-10 in the ileum and downregulated the cyclooxygenase COX-2 in the colon, suggesting an anti-inflammatory/regulatory activity. MIMBb23sg significantly affected the expression of the main gene involved in serotonin synthesis (TPH1) and the gene coding for the serotonin reuptake protein (SERT) in the ileum and colon, suggesting a potential propulsive effect toward the distal part of the gut, whereas the impact of MIMLh5 and DG on serotonergic genes suggested an effect toward motility control. The three probiotics decreased the expression of the permeability marker zonulin in gut distal sites. This preliminary in vivo study demonstrated the safety of the tested probiotic strains and their common ability to modulate the intestinal microbiota. The probiotics affected host gene expression in a strain-specific manner. Notably, the observed effects in the gut were site dependent. This study provides a rationale for investigating the effects of probiotics on the serotonergic system, which is a topic still widely unexplored.

scholarly journals Heavy Water Reduces GFP Expression in Prokaryotic Cell-Free Assays at the Translation Level While Stimulating Its Transcription

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Luisa S. Hohlefelder ◽  
Tobias Stögbauer ◽  
Madeleine Opitz ◽  
Thomas M. Bayerl ◽  
Joachim O. Rädler
Keyword(s):  
Gene Expression ◽  
Heavy Water ◽  
Expression System ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Gfp Expression ◽  
Antiproliferative Agent ◽  
Underlying Mechanisms ◽  
The Impact

Thein vitroproliferation of prokaryotic and eukaryotic cells is remarkably hampered in the presence of heavy water (D2O). Impairment of gene expression at the transcription or translation level can be the base for this effect. However, insights into the underlying mechanisms are lacking. Here, we employ a cell-free expression system for the quantitative analysis of the effect of increasing percentages of D2O on the kinetics ofin-vitroGFP expression. Experiments are designed to discriminate the rates of transcription, translation, and protein folding using pDNA and mRNA vectors, respectively. We find that D2O significantly stimulates GFP expression at the transcription level but acts as a suppressor at translation and maturation (folding) in a linear dose-dependent manner. At a D2O concentration of 60%, the GFP expression rate was reduced to 40% of an undisturbed sample. We observed a similar inhibition of GFP expression by D2O in a recombinantEscherichia colistrain, although the inhibitory effect is less pronounced. These results demonstrate the suitability of cell-free systems for quantifying the impact of heavy water on gene expression and establish a platform to further assess the potential therapeutic use of heavy water as antiproliferative agent.

Asymmetrical Attribution of Performance in China

Asian Survey ◽  
2020 ◽  
Vol 60 (5) ◽  
pp. 978-1003
Author(s):  
Jacqueline Chen Chen ◽  
Jun Xiang
Keyword(s):  
Economic Development ◽  
Local Governments ◽  
Central Government ◽  
Cultural Theory ◽  
Political Trust ◽  
Mediation Model ◽  
Multilevel Mediation ◽  
Dual Pathway ◽  
Underlying Mechanisms ◽  
The Impact

Existing studies of the impact of economic development on political trust in China have two major gaps: they fail to explain how economic development contributes to the hierarchical trust pattern, and they do not pay enough attention to the underlying mechanisms. In light of cultural theory and political control theory, we propose adapting performance theory into a theory of “asymmetrical attribution of performance” to better illuminate the case of China. This adapted theory leads to dual pathway theses: expectation fulfillment and local blaming. Using a multilevel mediation model, we show that expectation fulfillment mainly upholds trust in the central government, whereas local blaming undermines trust in local governments. We also uncover a rural–urban distinction in the dual pathway, revealing that both theses are more salient among rural Chinese.

Local mechanisms for acupoint sensitization in gall bladder meridian of foot shaoyang-a gene chip study

2019 ◽  
Vol 44 (2) ◽  
pp. 77-87
Author(s):  
Koichi Ishida ◽  
Liyue Qin ◽  
Ting Wang ◽  
Ying Lei ◽  
Weiwei Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gall Bladder ◽  
Interleukin 1 ◽  
Gene Chip ◽  
Molecular Evidence ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Bladder Meridian ◽  
Integrin Linked Kinase ◽  
Necrosis Factor

Acupuncture manipulations are clinically important to traditional Chinese medicine, yet the biological mechanisms have not been fully understood. This study aimed to investigate continuous stimulation-induced gene expression changes at stimulated and non-stimulated adjacent acupoints in the same meridian. Catgut embedding into acupoint (CEP) was conducted at acupoint Yanglingquan (gall bladder meridian of foot-shaoyang 34, GB34) of Sprague Dawley rats once or continuously for eight weeks, and gene expression changes at GB34 were assessed by gene chip array analysis 72 h after the last CEP treatment. A total of 688 genes exhibited opposite changes in expression between the two treatments, and 1,336 genes were regulated only by the eight-week CEP treatment. Ingenuity Pathway Analysis revealed that among these differentially regulated genes by one-time and eight-week CEP treatment, insulin-like growth factor-1 pathway and integrin-linked kinase pathway, and Wnt/~ catenin signaling pathway match the observed gene changes to predicted up/down regulation patterns. Upstream analysis further predicted six molecules, namely, tumor necrosis factor, interleukin 1~, interleukin la, kallikrein-related peptidase 5, protein kinase Ca, and catenin ~1. On the other hand, continuous eight-week CEP stimulation at acupoint Xuanzhong (GB39) caused similar changes in the expression of 32 genes at acupoints GB34 and Fengshi (GB31) on the same meridian. Taken together, our results provide the first molecular evidence for the local acupoints' mechanisms for acupoint sensitization theory, and implicate the existence of signaling pathways, either direct or indirect, between acupoints within the meridian GB.

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