scholarly journals Role of JAK-STAT Pathway in Broiler Chicks Fed with Chestnut Tannins

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 337
Author(s):  
Annah Lee ◽  
Gabriela Cardoso Dal Pont ◽  
Michele Battaglia ◽  
Ryan J. Arsenault ◽  
Michael H. Kogut
Keyword(s):  
Mrna Expression ◽  
Signaling Pathway ◽  
Immune Modulation ◽  
Cell Receptor ◽  
Host Immunity ◽  
Broiler Chicks ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Stat Pathway

The objective of this study was to identify the phosphorylation events associated with host immunity with the inclusion of chestnut tannins (ChT) in the diet. A total of 200 male day-of-hatch Cobb 500 chicks were randomly assigned to two treatment groups, totaling 50 chicks per pen per experiment (this study was repeated two times). The treatments were as follows: (1) control feed—normal starter feed (n = 50), and (2) 1% ChT inclusion feed (n = 50). The ceca were collected on each necropsy day for analysis via (1) a peptide array to provide tissue immunometabolism information from the host, and (2) quantitative PCR for mRNA expression. Of the top three immune pathways, the data identified the T-cell receptor signaling pathway, the chemokine signaling pathway, and the JAK-STAT signaling pathway. The results showed significantly altered phosphorylation of JAK and STAT peptides within the JAK-STAT pathway. These results support the mRNA expression data with the upregulated IL-6 response, due to the significant phosphorylation of IL6ST, JAK, and STAT peptides. In regard to immune modulation, ChT appear to influence host immunity via an IL-6 mediated response which could be beneficial in host defenses against pathogens at the early stages of broiler growth and development. Therefore, it is suggested that the role of the JAK-STAT pathway is altered by including ChT in the diet.

scholarly journals The clinical significance of glutathione peroxidase 2 in glioblastoma multiforme

2021 ◽  
Vol 12 (1) ◽  
pp. 032-039
Author(s):  
Bangming Guo ◽  
Wenjuan Liao ◽  
Shusheng Wang
Keyword(s):  
Glioblastoma Multiforme ◽  
Glutathione Peroxidase ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Clinical Significance ◽  
Cancer Cell ◽  
Statistical Significance ◽  
Adult Brain ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway

Abstract Background Glioblastoma multiforme (GBM) is the leading cause of death among adult brain cancer patients. Glutathione peroxidase 2 (GPX2), as a factor in oxidative stress, plays an important role in carcinogenesis. However, its role in GBM has not been well established. The study aimed to investigate the clinical significance of GPX2 with GBM prognosis. Methods Data of GBM and healthy individuals were retrospectively collected from oncomine, cancer cell line encyclopedia (CCLE), gene expression profiling interactive analysis (GEPIA), UALCAN, and Human Protein Atlas. GPX2 mRNA expression was first assessed across various cancer types in oncomine and cancer cell lines from CCLE. The mRNA expression of GPX2 was compared between normal and GBM tissues using GEPIA (normal = 207; GBM = 163) and UALCAN (normal = 5; GBM = 156). The GPX2 methylation was analyzed using data from UALCAN (normal = 2; GBM = 140). The prognostic value of GPX2 in GBM was explored in GEPIA and UALCAN using Kaplan–Meier method. STRING database was used to construct protein–protein interaction (PPI) network and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Statistical significance was set as <0.05. Results The current study revealed no significant differences in GPX2 expression between normal and GBM from GEPIA data (P > 0.05) and UALCAN (P = 0.257). Patients with higher GPX2 intended to have a poorer prognosis (P = 0.0089). The KEGG pathways found that chemokine-signaling pathway were the more preferred. Conclusions The findings demonstrated that GPX2 might be a potential diagnosis and prognostic indicator for GBM. Chemokine-signaling pathway may be involved in GPX2 function.

scholarly journals Specific Differentially Methylated and Expressed Genes in People with Longevity Family History

2021 ◽  
Author(s):  
Chunhong LI ◽  
Qingqing NONG ◽  
Bin GUAN ◽  
Haoyu HE ◽  
Zhiyong ZHANG
Keyword(s):  
Family History ◽  
Signaling Pathway ◽  
Killer Cell ◽  
Cell Receptor ◽  
Human Longevity ◽  
Chemokine Signaling ◽  
Differentially Methylated Genes ◽  
Receptor Signaling Pathway ◽  
Chemokine Signaling Pathway ◽  
And Control

Background: We attempt to identify specific differentially methylated and expressed genes in people with longevity family history, it will contribute to discover significant features about human longevity. Methods: A prevalence study was conducted during October 2017 to January 2019 in Bama County of Guangxi, China and individuals were recruited and grouped into longevity family (n=60) and non-longevity family (n=60) to identify differentially methylated genes (DMGs). The expression profile dataset GSE16717 was downloaded from the GEO database in which individuals were divided into 3 groups, namely longevity (n=50), longevity offspring (n=50) and control (n=50) for identifying differentially expressed genes (DEGs). It was considered significantly different when P or adjusted P0.05. Results: In total, 117 longevity-related hypermethylated genes enriched in interleukin secretion/production regulation, chemokine signaling pathway and natural killer cell-mediated cytotoxicity. Another 296 significant key longevity-related DEGs primarily involved in protein binding, nucleus, cytoplasm, T cell receptor signaling pathway and Metabolic pathway, H19 and PFKFB4 were found to be both methylated and downregulated in people with longevity family history. Conclusion: Human longevity-specific genes involve in many immunity regulations and cellular immunity pathways, H19 and PFKFB4 show hypermethylated and suppressed status in people with longevity family history and might serve as longevity candidate genes.

scholarly journals Network-Based Association Study of Obesity and Type 2 Diabetes with Gene Expression Profiles

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Siyi Zhang ◽  
Bo Wang ◽  
Jingsong Shi ◽  
Jing Li
Keyword(s):  
Type 2 Diabetes ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cell Receptor ◽  
Mapk Signaling ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway

The increased prevalence of obesity and type 2 diabetes (T2D) has become an important factor affecting the health of the human. Obesity is commonly considered as a major risk factor for the development of T2D. However, the molecular mechanisms of the disease relations are not well discovered yet. In this study, the combination of multiple differential expression profiles and a comprehensive biological network of obesity and T2D allowed us to identify and compare the disease-responsive active modules and subclusters. The results demonstrated that the connection between obesity and T2D mainly relied on several pathways involved in the digestive metabolism, immunization, and signal transduction, such as adipocytokine, chemokine signaling pathway, T cell receptor signaling pathway, and MAPK signaling pathways. The relationships of almost all of these pathways with obesity and T2D have been verified by the previous reports individually. We also found that the different parts in the same pathway are activated in obesity and T2D. The association of cancer, obesity, and T2D was identified too here. As a conclusion, our network-based method not only gives better support for the close connection between obesity and T2D, but also provides a systemic view in understanding the molecular functions underneath the links. It should be helpful in the development of new therapies for obesity, T2D, and the associated diseases.

scholarly journals LncRNA and transcriptomic analysis of fetal membrane revealed potential targets involved in oligohydramnios

2019 ◽  
Author(s):  
Yu-hua Ou ◽  
Yu-kun Liu ◽  
Li-qiong Zhu ◽  
Man-qi Chen ◽  
Xiao-chun Yi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Tissue Growth ◽  
Differentially Expressed ◽  
Fetal Membrane ◽  
Ras Signaling ◽  
Chromosome 2 ◽  
Chemokine Signaling ◽  
Wide Range ◽  
Chemokine Signaling Pathway

Abstract The challenge of oligohydramnios study is multiple causes of oligohydramnios. Long noncoding RNAs (lncRNAs) is a set of RNAs that has been proved to function in multiple biological process. Currently, little is know about their expression and possible role in oligohydramnios. Total RNA was isolated from fetal membranes ressected from oligohydramnios pregnant women (OR) and normal amniotic fluid control (Normal).RNA-sequencing (RNA-seq) obtain that a total of 801 lncRNAs and 367 mRNAs were differentially expressed in OR. Of which, 638 lncRNAs and 189 mRNAs were upregulated, and 163 lncRNAs and 178 mRNAs were downregulated. Of these lncRNAs, 566 of them were intergenic lncRNA, 351 were intronic antisense lncRNA，and 300 natural antisense. The differentially expressed lncRNA were primary located in chromosome 2, 1 and 11. KEGG enrichment pathways revealed the differential expressed mRNAs were enriched in pathway in cancer, Ras signaling pathway, TNF signaling pathway, focal adhesion, and chemokine signaling pathway. The qRT-PCR result confirmed that LINC00515 and RP11-388P9.2 were upregulated in OR. Furthermore, the constructed lncRNA-miRNA-mRNA regulatory network revealed TNR, CFTR, ABCC2, ABCA12, and COL9A2 as the candidate targets of LINC00515 and RP11-388P9.2. A wide range of lncRNAs were alert in OR, in particularly, LINC00515 and RP11-388P9.2 were confirmed to be uprgulated in OR, and their predicted downstream targets were transport and tissue growth and development associated. Further study focused on the role of differential expressed lncRNAs such as LINC00515 and RP11-388P9.2 would provide more insight into the pathophysiology in OR.

scholarly journals Investigation of Potential Genetic Biomarkers and Molecular Mechanism of Ulcerative Colitis Utilizing Bioinformatics Analysis

2019 ◽  
Author(s):  
Jiaqi Zhang ◽  
Xue Wang ◽  
Lin Xu ◽  
Zedan Zhang ◽  
Fengyun Wang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Gene Therapy ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Functional Enrichment ◽  
Hub Genes ◽  
Amyloid A ◽  
Chemokine Signaling ◽  
Chemokine Signaling Pathway ◽  
Potential Biomarkers

Abstract Objectives: To reveal the molecular mechanisms of ulcerative colitis (UC) and provide potential biomarkers for UC gene therapy. Methods: We downloaded the GSE87473 microarray dataset from the Gene Expression Omnibus (GEO) and identified the differentially expressed genes (DEGs) between UC samples and normal samples. Then ,a module partition analysis was performed based on a weighted gene co-expression network analysis (WGCNA),followed by pathway and functional enrichment analyses. Furthermore, we investigated the hub genes . At last, data validation was performed to ensure the reliability of the hub genes. Results: Between UC group and normal group, 988 DEGs were investigated . The DEGs were clustered into 5 modules using WGCNA. These DEGs were mainly enriched in functions such as the immune response, the inflammatory response and chemotaxis, and they were mainly enriched in KEGG pathways such as the cytokine-cytokine receptor interaction , chemokine signaling pathway, and complement and coagulation cascades. The hub genes, including dual oxidase maturation factor 2(DUOXA2), serum amyloid A (SAA) 1 and SAA2, TNFAIP3-interacting protein 3(TNIP3), C-X-C motif chemokine (CXCL1), solute carrier family 6 member 14(SLC6A14) and complement decay-accelerating factor (CD antigen CD55),were revealed as potential tissue biomarkers for UC diagnosis or treatment. Conclusions: This study provides supportive evidence that DUOXA2, A-SAA, TNIP3, CXCL1, SLC6A14 and CD55 might be used as potential biomarkers for tissue biopsy of UC, especially SLC6A14 and CD55, which may be new targets for UC gene therapy. Moreover, the DUOX2/DUOXA2, NF-κB /TNIP3 and CXCL1/CXCR2 pathways might play an important role in the progression of UC through the chemokine signaling pathway and inflammatory response.

scholarly journals Mutational burden of hepatoblastomas: a role for the CX3CL1/CX3CR1 chemokine signaling pathway

2019 ◽  
Author(s):  
Talita Ferreira Marques Aguiar ◽  
Maria Prates Rivas ◽  
Silvia Costa ◽  
Tatiane Rodrigues ◽  
Juliana Sobral de Barros ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Tumor Cells ◽  
Somatic Mutations ◽  
Chemotherapy Response ◽  
Mutational Signature ◽  
Relative Paucity ◽  
Chemokine Signaling ◽  
Cancer Types ◽  
Negative Tumor ◽  
Chemokine Signaling Pathway

ABSTRACTBackgroundHepatoblastoma is an embryonal liver tumor supposed to arise from the impairment of hepatocyte differentiation during embryogenesis. CTNNB1 is the only recurrently mutated gene, and this relative paucity of somatic mutations poses a challenge to risk stratification and development of targeted therapies.MethodsIn this study, we investigated by exome sequencing the burden of somatic mutations in a cohort of 10 hepatoblastomas, including a congenital case.ResultsOur data disclosed a low mutational background with only three recurrently mutated genes: CTNNB1 and two novel candidates, CX3CL1 and CEP164. The major finding was a recurrent mutation (A235G) identified in two hepatoblastomas at the CX3CL1 gene; evaluation of RNA and protein expression revealed up-regulation of CX3CL1 in tumors. The analysis was replicated in two independents cohorts, substantiating that an activation of the CX3CL1/CX3CR1 pathway occurs in hepatoblastomas, with a predominance of these proteins in the cytoplasm of tumor cells. These proteins were not detected in the infiltrated lymphocytes of inflammatory regions of the tumors, in which they should be expressed in normal conditions, whereas necrotic regions exhibited negative tumor cells, but strongly positive infiltrated lymphocytes. Our data suggested that CX3CL1/CX3CR1 upregulation may be a common feature of hepatoblastomas, potentially related to chemotherapy response and progression. In addition, three mutational signatures were identified in hepatoblastomas, two of them with predominance of either the COSMIC signatures 1 and 6, found in all cancer types, or the COSMIC signature 29, related only with tobacco chewing habit; a third novel mutational signature presented an unspecific pattern with an increase of C>A mutations.ConclusionsOverall, we present here evidence that CX3CL1/CX3CR1 chemokine signaling pathway is likely involved with hepatoblastoma tumorigenesis or progression, besides reporting a novel mutational signature specific to a hepatoblastoma subset.

Sign in / Sign up

Export Citation Format

Share Document