scholarly journals Transcriptome Analysis Revealed Potential Mechanisms of Resistance to Trichomoniasis gallinae Infection in Pigeon (Columba livia)

2021 ◽  
Vol 8 ◽  
Author(s):  
Jingwei Yuan ◽  
Aixin Ni ◽  
Yunlei Li ◽  
Shixiong Bian ◽  
Yunjie Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Columba Livia ◽  
Receptor Interaction ◽  
Host Animal ◽  
Main Site ◽  
P53 Signaling ◽  
Immune Related Genes ◽  
Focal Adhesion Pathway

Trichomoniasis gallinae (T. gallinae) is one of the most pathogenic parasites in pigeon, particularly in squabs. Oral cavity is the main site for the host-parasite interaction. Herein, we used RNA-sequencing technology to characterize lncRNA and mRNA profiles and compared transcriptomic dynamics of squabs, including four susceptible birds (S) from infected group, four tolerant birds (T) without parasites after T. gallinae infection, and three birds from uninfected group (N), to understand molecular mechanisms underlying host resistance to this parasite. We identified 29,809 putative lncRNAs and characterized their genomic features subsequently. Differentially expressed (DE) genes, DE-lncRNAs and cis/trans target genes of DE-lncRNAs were further compared among the three groups. The KEGG analysis indicated that specific intergroup DEGs were involved in carbon metabolism (S vs. T), metabolic pathways (N vs. T) and focal adhesion pathway (N vs. S), respectively. Whereas, the cis/trans genes of DE-lncRNAs were enriched in cytokine-cytokine receptor interaction, toll-like receptor signaling pathway, p53 signaling pathway and insulin signaling pathway, which play crucial roles in immune system of the host animal. This suggests T. gallinae invasion in pigeon mouth may modulate lncRNAs expression and their target genes. Moreover, co-expression analysis identified crucial lncRNA-mRNA interaction networks. Several DE-lncRNAs including MSTRG.82272.3, MSTRG.114849.42, MSTRG.39405.36, MSTRG.3338.5, and MSTRG.105872.2 targeted methylation and immune-related genes, such as JCHAIN, IL18BP, ANGPT1, TMRT10C, SAMD9L, and SOCS3. This implied that DE-lncRNAs exert critical influence on T. gallinae infections. The quantitative exploration of host transcriptome changes induced by T. gallinae infection broaden both transcriptomic and epigenetic insights into T. gallinae resistance and its pathological mechanism.

scholarly journals Integrated Transcriptome Analysis of microRNA and mRNA in Mouse Skin Derived Precursors (SKPs) and SKP Derived Fibroblast (SFBs) by RNA-Seq

2019 ◽  
Vol 20 (1) ◽  
pp. 49-60 ◽  
Author(s):  
Rongying Zhou ◽  
Yujie Mao ◽  
Lidan Xiong ◽  
Li Li
Keyword(s):  
Mrna Expression ◽  
Signaling Pathway ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Gene List ◽  
Mouse Skin ◽  
Cytokine Receptor ◽  
Receptor Interaction ◽  
Integrated Analysis

Background: Skin-derived precursors (SKPs) display the characteristics of self-renewal and multilineage differentiation. Objective: The study aimed to explore the molecular mechanisms of mouse SKPs differentiation into SKP-derived fibroblasts (SFBs). Methods: We compared the microRNA (miRNA) profile in mouse SKPs and SFBs by RNA sequencing. Real-time quantitative reverse transcription PCR (qRT-PCR) was performed to validate the miRNA expression. The integrated analysis of miRNA and mRNA expression data was performed to explore the potential crosstalk of miRNA-mRNA in SKP differentiation. Results: 207 differentially expressed miRNAs and 835 miRNA target genes in the gene list of integrated mRNA expression profiling were identified. Gene Ontology (GO) enrichment analysis revealed that cell differentiation and cell proliferation process were significantly enriched. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed the target genes were significantly most enriched in the cytokine-cytokine receptor interaction, cancer pathways and axon guidance signaling pathway. The most upregulated and downregulated target genes were involved in the Wnt, Notch, cytokine- cytokine receptor interaction, TGF-β, p53 and apoptotic signaling pathway. The miRNAmRNA regulatory networks and 507 miRNA-mRNA pairs were constructed. Seven miRNAs (miR- 486-3p, miR-504-5p, miR-149-3p, miR-31-5p, miR-484, miR-328-5p and miR-22-5p) and their target genes Wnt4, Dlx2, Sema4f, Kit, Kitl, Inpp5d, Igfbp3, Prdm16, Sfn, Irf6 and Clu were identified as miRNA-mRNA crosstalk pairs. Conclusion: These genes and signaling pathways might control SKPs proliferation and SKPs differentiation into SFBs during the process of SKPs differentiation, which might promote the application of SKPs in the clinical treatment of skin-related diseases by regulating SKPs proliferation and SKPs differentiation.

scholarly journals Anticancer Effects of Emodin on HepG2 Cell: Evidence from Bioinformatic Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Rui-sheng Zhou ◽  
Xiong-Wen Wang ◽  
Qin-feng Sun ◽  
Zeng Jie Ye ◽  
Jian-wei Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Ion Concentration ◽  
Receptor Interaction ◽  
Pathway Enrichment Analysis ◽  
Mrna Levels ◽  
Hub Genes ◽  
Positive Regulation

Hepatocellular carcinoma (HCC) is a primary cause of cancer-related death in the world. Despite the fact that there are many methods to treat HCC, the 5-year survival rate of HCC is still at a low level. Emodin can inhibit the growth of HCC cells invitroand invivo. However, the gene regulation of emodin in HCC has not been well studied. In our research, RNA sequencing technology was used to identify the differentially expressed genes (DEGs) in HepG2 cells induced by emodin. A total of 859 DEGs were identified, including 712 downregulated genes and 147 upregulated genes in HepG2 cells treated with emodin. We used DAVID for function and pathway enrichment analysis. The protein-protein interaction (PPI) network was constructed using STRING, and Cytoscape was used for module analysis. The enriched functions and pathways of the DEGs include positive regulation of apoptotic process, structural molecule activity and lipopolysaccharide binding, protein digestion and absorption, ECM-receptor interaction, complement and coagulation cascades, and MAPK signaling pathway. 25 hub genes were identified and pathway analysis revealed that these genes were mainly enriched in neuropeptide signaling pathway, inflammatory response, and positive regulation of cytosolic calcium ion concentration. Survival analysis showed that LPAR6, C5, SSTR5, GPR68, and P2RY4 may be involved in the molecular mechanisms of emodin therapy for HCC. A quantitative real-time PCR (qRT-PCR) assay showed that the mRNA levels of LPAR6, C5, SSTR5, GPR68, and P2RY4 were significantly decreased in HepG2 cells treated with emodin. In conclusion, the identified DEGs and hub genes in the present study provide new clues for further researches on the molecular mechanisms of emodin.

scholarly journals Nanopore Long-Read Transcriptomics Profiling Reveals Gene Expression Signatures of Mouse Tumor Endothelial Cells 2H-11

2021 ◽  
Author(s):  
Yuanyuan Tian ◽  
Jiao Zhao ◽  
Ju Huang ◽  
Haiying Zhang ◽  
Fushun Ni ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Antigen Processing ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Receptor Interaction ◽  
Glutathione Metabolism ◽  
Signal Pathways ◽  
Mouse Tumor ◽  
Tumor Endothelial Cells

Abstract Background:Tumor endothelial cells (TECs) play an indispensable role in tumor growth and metastasis. Compared with normal endothelial cells (NECs), TECs exhibit unique phenotypic and functional heterogeneity in terms of metabolism, genetics, and transcriptomics. It is not only the key to coordinate tumor angiogenesis, but also an important factor of immune regulation in the tumor microenvironment. In recent years, the role of TECs in tumor metabolism and invasion has been continuously reported. However, the research on the mechanism behind the complex functions of TECs is still at the basic stage. We use Oxford Nanopore Technology (ONT) three-generation full-length transcriptome sequencing to detect all genetic structural changes in the transcriptome of mouse TECs 2H-11 and mouse NECs SVEC4-10.Results: In Tumor endothelial cells 2H-11,1847genes are up-regulated and 1202 genes are down-regulated. According to the Gene ontology (GO) enrichment analysis of differentially expressed genes (DEGs), we found that different functional trends related to metabolic processes, developmental processes, localization, immune system processes, and locomotion are the main reasons for the differences. DEGs are mainly enriched in signal pathways related to cancer, immunity and metabolism, involving Pathways in cancer,Antigen processing and presentation , Proteoglycans in cancer, Focal adhesion, MAPK signaling pathway ,Protein digestion and absorption，ECM-receptor interaction，PI3K-Akt signaling pathway and Glutathione metabolism. We also obtained the structural variation of transcripts such as alternative splicing, gene fusion, and alternative polyadenylation and accurately quantified the expression of the transcript. Some of our results have been confirmed in other documents. But other data have not been reported yet, which is the focus of our future exploration.Conclusion: We try to use transcriptomics and bioinformatics methods to characterize tumor endothelial cell-related genes and signaling pathways.It could help better understand the molecular mechanisms of tumor endothelial cells involved in tumorigenesis and development. DEGs in key pathways may be potential diagnostic markers or therapeutic targets of TECs. Our data also provide useful genetic resources for improving the genome and transcriptome annotations of TECs and NECs.

scholarly journals Disorder Genes Regulate the Progression of Ischemic Stroke through the NF-κB Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Wei Wei ◽  
Wenqiang Xin ◽  
Yufeng Tang ◽  
Zhonglun Chen ◽  
Yue Heng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Differential Gene ◽  
Coexpression Network Analysis ◽  
Geo Database ◽  
Differential Genes

Stroke is an acute cerebrovascular disease, including ischemic and hemorrhagic stroke. Stroke is the second leading cause of death after ischemic heart disease, which accounts for 9% of the global death toll. To explore the molecular mechanisms of the effects of the dysregulated factors, in the GEO database, we obtained transcriptome data from 24 h/72 h of mice with ischemic stroke and 24 h/72 h of normal mice. We then performed differential gene analysis, coexpression analysis, enrichment analysis, and regulator prediction bioinformatics analysis to identify the potential genes. We made a comparison between the ischemic stroke 72 h and the ischemic stroke for 24 h, and 5103 differential genes were obtained ( p < 0.05 ). Four functional barrier modules were obtained by weighted gene coexpression network analysis. The critical genes of each module were ASTL, Zfp472, Fmr1 gene, and Nap1l1. The results of the enrichment analysis showed ncRNA metabolism, microRNAs in cancer, and biosynthesis of amino acids. These three functions and pathways have the most considerable count value. The regulators of the regulatory dysfunction module were predicted by pivotal analysis of TF and noncoding RNA, and critical regulators including NFKB1 (NF-κB1), NFKBIA, CTNNB1, and SP1 were obtained. Finally, the pivotal target gene found that CTNNB1, NFKB1, NFKBia, and Sp1 are involved in 18, 32, 2, and 60 target genes, respectively. Therefore, we believe that NFKB1 and Sp1 have a potential role in the progression of ischemic stroke. The NFKB signaling pathway promotes inflammatory cytokines and regulates the progression of ischemic stroke.

scholarly journals The molecular mechanisms associated with PIN7, a protein-protein interaction network of seven pleiotropic proteins

2019 ◽  
Author(s):  
Jarmila Nahálková
Keyword(s):  
Signaling Pathway ◽  
Protein Interaction ◽  
Protein Interaction Network ◽  
Molecular Mechanisms ◽  
Interaction Network ◽  
Protein Protein Interaction ◽  
P53 Signaling ◽  
Age Related ◽  
P53 Signaling Pathway ◽  
Protein Protein Interaction Network

The protein-protein interaction network of seven pleiotropic proteins (PIN7) contains proteins with multiple functions in the aging and age-related diseases (TPPII, CDK2, MYBBP1A, p53, SIRT6, SIRT7, and BSG). At the present work, the pathway enrichment, the gene function prediction and the protein node prioritization analysis were applied for the examination of main molecular mechanisms driving PIN7 and the extended network. Seven proteins of PIN7 were used as an input for the analysis by GeneMania, a Cytoscape application, which constructs the protein interaction network. The software also extends it using the interactions retrieved from databases of experimental and predicted protein-protein and genetic interactions. The analysis identified the p53 signaling pathway as the most dominant mediator of PIN7. The extended PIN7 was also analyzed by Cytohubba application, which showed that the top-ranked protein nodes belong to the group of histone acetyltransferases and histone deacetylases. These enzymes are involved in the reverse epigenetic regulation mechanisms linked to the regulation of PTK2, NFκB, and p53 signaling interaction subnetworks of the extended PIN7. The analysis emphasized the role of PTK2 signaling, which functions upstream of the p53 signaling pathway and its interaction network includes all members of the sirtuin family. Further, the analysis suggested the involvement of molecular mechanisms related to metastatic cancer (prostate cancer, small cell lung cancer), hemostasis, the regulation of the thyroid hormones and the cell cycle G1/S checkpoint. The additional data-mining analysis showed that the small protein interaction network MYBBP1A-p53-TPPII-SIRT6-CD147 controls Warburg effect and MYBBP1A-p53-TPPII-SIRT7-BSG influences mTOR signaling and autophagy. Further investigations of the detail mechanisms of these interaction networks would be beneficial for the development of novel treatments for aging and age-related diseases.

scholarly journals Identification of Key Genes and Pathways Associated with Mast Cells Resting in Meningioma

2020 ◽  
Author(s):  
Hui Xie ◽  
Xiao-hui Ding ◽  
Ce Yuan ◽  
Jin-jiang Li ◽  
Zhao-yang Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mast Cells ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
Risk Model ◽  
Kegg Pathway ◽  
Expression Profiles ◽  
Receptor Interaction ◽  
Key Genes

Abstract Background: To identify candidate key genes and pathways related to mast cells resting in meningioma and the underlying molecular mechanisms of meningioma.Methods: Gene expression profiles of GSE43290 and GSE16581 datasets were obtained from the Gene Expression Omnibus (GEO) database. GO and KEGG pathway enrichments of DEGs were analyzed using the ClusterProfiler package in R. The protein-protein interaction network (PPI), and TF-miRNA- mRNA co-expression networks were constructed. Further, the difference in immune infiltration was investigated using the CIBERSORT algorithm.Results: A total of 1499 DEGs were identified between tumor and normal controls. The analysis of the immune cell infiltration landscape showed that the probability of distribution of memory B cells, regulatory T cells (Tregs), and resting mast cells in tumor samples were significantly higher than those in the controls. Moreover, through WGCNA analysis, the module related to mast cells resting contained 158 DEGs, and KEGG pathway analysis revealed that the DEGs were dominant in the TNF signaling pathway, cytokine-cytokine receptor interaction, and IL-17 signaling pathway. Survival analysis of hub genes related to mast cells resting showed that the risk model was constructed based on 9 key genes. The TF-miRNA- mRNA co-regulation network, including MYC-miR-145-5p, TNFAIP3-miR-29c-3p, and TNFAIP3-hsa-miR-335-3p, were obtained. Further, 36 nodes and 197 interactions in the PPI network were identified. Conclusions: The results of this study revealed candidate key genes, miRNAs, and pathways related to mast cells resting involved in meningioma development, providing potential therapeutic targets for meningioma treatment.

scholarly journals Analysis of Transcriptomic Changes in Bovine Endometrial Stromal Cells Treated With Lipopolysaccharide

2020 ◽  
Vol 7 ◽  
Author(s):  
Xuefen Ding ◽  
Haimiao Lv ◽  
Lixin Deng ◽  
Wenju Hu ◽  
Zhan Peng ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Stromal Cells ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Interleukin 12 ◽  
Receptor Interaction ◽  
Control Group ◽  
Toll Like Receptor ◽  
Endometrial Stromal Cells

Endometritis adversely affects the ability of cattle to reproduce and significantly reduces milk production. The is mainly composed of epithelial and stromal cells, and they produce the first immune response to invading pathogens. However, most of the epithelial cells are disrupted, and stromal cells are exposed to an inflammatory environment when endometritis occurs, especially postpartum. Many bacteria and toxins start attacking stromal cell due to loss of epithelium, which stimulates Toll-like receptor (TLRs) on stromal cells and causes upregulated expression of cytokines. Understanding the genome-wide characterization of bovine endometritis will be beneficial for prevention and treatment of endometritis. In this study, whole-transcriptomic gene changes in bovine endometrial stromal cells (BESCs) treated with LPS were compared with those treated with PBS (control group) and were analyzed by RNA sequencing. Compared with the control group, a total of 366 differentially expressed genes (DEGs) were identified in the LPS-induced group (234 upregulated and 132 downregulated genes), with an adjusted P &lt; 0.05 by DESeq. Gene Ontology (GO) enrichment analysis revealed that DEGs were most enriched in interleukin-1 receptor binding, regulation of cell activation, and lymphocyte-activated interleukin-12 production. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed DEGs were most enriched in the TNF signaling pathway, Toll-like receptor signaling pathway, cytokine–cytokine receptor interaction, NF-κB signaling pathway, and chemokine signaling pathway. The results of this study unraveled BESCs affected with LPS transcriptome profile alterations, which may have a significant effect on treatment inflammation by comprehending molecular mechanisms and authenticating unique genes related to endometritis.

scholarly journals Identification of miRNA-mRNA Crosstalk in Respiratory Syncytial Virus- (RSV-) Associated Pediatric Pneumonia through Integrated miRNAome and Transcriptome Analysis

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Xu Zhang ◽  
Feng Huang ◽  
Diyuan Yang ◽  
Tao Peng ◽  
Gen Lu
Keyword(s):  
Respiratory Syncytial Virus ◽  
Signaling Pathway ◽  
Whole Blood ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Expression Profiles ◽  
Mapk Signaling ◽  
Design Strategies ◽  
Pediatric Pneumonia ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is the most common respiratory virus and is associated with pediatric pneumonia, causing bronchiolitis and significant mortality in infants and young children. MicroRNAs (miRNAs) are endogenous noncoding small RNAs that function in gene regulation and are associated with host immune response and disease progression. In the present study, we profiled the global transcriptome and miRNAome of whole blood samples from children with mild or severe RSV-associated pneumonia, aiming to identify the potential biomarkers and investigate the molecular mechanisms of severe RSV-associated pediatric pneumonia. We found that expression profiles of whole blood microRNAs and mRNAs were altered and distinctly different in children with severe RSV-associated pneumonia. In particular, the four most significantly upregulated miRNAs in children with severe RSV-associated pneumonia were hsa-miR-1271-5p, hsa-miR-10a-3p, hsa-miR-125b-5p, and hsa-miR-30b-3p. The severe RSV-associated pneumonia-specific differentially expressed miRNA target interaction network was also contrasted. These target genes were further analyzed with Gene Ontology enrichment analysis. We found that most of the target genes were involved in inflammatory and immune responses, including the NF-κB signaling pathway, the MAPK signaling pathway, and T cell receptor signaling. Our findings will contribute to the identification of biomarkers and new drug design strategies to treat severe RSV-associated pediatric pneumonia.

scholarly journals Blood Gene Expression Profile Study Revealed the Activation of Apoptosis and p53 Signaling Pathway May Be the Potential Molecular Mechanisms of Ionizing Radiation Damage and Radiation-Induced Bystander Effects

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091418
Author(s):  
Guangyao He ◽  
Anzhou Tang ◽  
Mao Xie ◽  
Wei Xia ◽  
Pengcheng Zhao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Network Analysis ◽  
Ionizing Radiation ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Enrichment Analysis ◽  
P53 Signaling ◽  
Gene Correlation ◽  
Radiation Induced ◽  
P53 Signaling Pathway

Radiotherapy is an effective treatment for local solid tumors, but the mechanism of damage to human body caused by radiation therapy needs further study. In this study, gene expression profiles of human peripheral blood samples exposed to different doses and rates of ionizing radiation (IR) were used for bioinformatics analysis to investigate the mechanism of IR damage and radiation-induced bystander effect (RIBE). Differentially expressed genes analysis, weighted gene correlation network analysis, functional enrichment analysis, hypergeometric test, gene set enrichment analysis, and gene set variation analysis were applied to analyze the data. Moreover, receiver operating characteristic curve analysis was performed to identify core genes of IR damage. Weighted gene correlation network analysis identified 3 modules associated with IR damage, 2 were positively correlated and 1 was negatively correlated. The analysis showed that the positively correlated modules were significantly involved in apoptosis and p53 signaling pathway, and ESR1, ATM, and MYC were potential transcription factors regulating these modules. Thus, the study suggested that apoptosis and p53 signaling pathway may be the potential molecular mechanisms of IR damage and RIBE, which could be driven by ESR1, ATM, and MYC.

scholarly journals Differential Expression of MicroRNAs and their Possible Roles in Patients with Chronic Idiopathic Urticaria and Active Hives

2017 ◽  
Vol 8 (2) ◽  
pp. ar.2017.8.0199 ◽  
Author(s):  
Ching-Kow E. Lin ◽  
John S. Kaptein ◽  
Javed Sheikh
Keyword(s):  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Chronic Idiopathic Urticaria ◽  
Receptor Interaction ◽  
Messenger Rnas ◽  
P53 Signaling ◽  
Autoimmune Urticaria ◽  
Complicated Skin ◽  
P21 Activated Kinase

Background Chronic idiopathic urticaria (CIU) is a complicated skin disease with unknown pathophysiology. MicroRNAs (miRNA) have been shown to be active in cellular regulation. The goal of this pilot study was to examine whether miRNAs may be involved in the regulation of CIU or as biomarkers for CIU. Methods Four groups of three patients each were selected: patients with either active hives or no hives and with positive or negative chronic urticaria (CU) index results. MiRNAs were isolated from patient plasma and analyzed by using miRNA microarray technology to determine the amount of each of the 2567 known human miRNAs. Results A total of 16 miRNAs were found to be differentially expressed in patients with active hives. Among them, five (2355–3p, 4264, 2355–5p, 29c-5p, and 361–3p) were significantly increased in samples with positive CU index results, which could be useful biomarkers for patients with chronic autoimmune urticaria. The miRNA data bases were used to find the targets of these selected miRNA sequences. These potential targets were then compared against a list of 154 urticaria-related genes. Twenty-five genes were found to match. These included eight that were significantly downregulated and eight that were significantly upregulated; however, seven of the eight downregulated genes (FBXL20, OPHN1, YPEL2, STARD9, EZH1, KLHL24, ING4) and five of the eight upregulated genes (BYSL, PNO1, ADAMTS9, STEAP4, SRGN) have no reported roles in signaling. For the 13 genes with reported roles in signaling, the following pathways were found: transforming growth factor beta signaling pathway (NRC31, KITLG, THBS1, CCL2), glucocorticoid receptor signaling pathway (NR3C1, SELE, CCL2), p53 signaling pathway (CCNG2, THBS1, CCL2), p21-activated kinase pathway (PAK1IP1, KITLG, CCL2), phosphoinositide-3 kinase protein kinase B signaling pathway (KITLG, CHRM, THBS1), and neuroactive ligand-receptor interaction (NRC31, HRH1, CHRM), which could play important roles in CIU. Conclusion A better understanding of those genes with undefined function and simultaneous quantitation of both miRNAs and messenger RNAs are needed to fully understand CIU disease.

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