Association between the &lt;b&gt;&lt;i&gt;IFNA1 &lt;/i&gt;&lt;/b&gt;(-2C&amp;#x2192;T) Polymorphism and Increased &lt;b&gt;&lt;i&gt;IFNAR1 &lt;/i&gt;&lt;/b&gt;Gene Expression Levels in Chronic Hepatitis B Infection

Santos, Joelma Carvalho; Deus, Dayse Maria Vasconcelos de; Moura, Izolda; Lopes, Edmundo Pessoa; Alves, Maria Rosileide Bezerra; Coêlho, Maria Rosângela Cunha Duarte

doi:10.1159/000444365

Cited by 3 publications

(3 citation statements)

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“…IFNA1, as one of the interferons, has been widely reported to have antiviral action and affects the adaptive immune response, which is involving dendritic cells and NK cells, as well as lymphocytes (Platanias, ; Tang, ). Santos et al () investigated that upregulation of the IFNAR1 gene and downregulation of IFNA1 might have a function on the pathogenesis of chronic infection. Overexpression of IRF‐I gene also has been found during the ATRA induction of leukemic cells and acts as a potential candidate gene for antitumor effect (Matikainen, Ronni, Hurme, Pine, & Julkunen, ).…”

Section: Discussionmentioning

confidence: 99%

Downregulation of long noncoding RNA LOC101928134 inhibits the synovial hyperplasia and cartilage destruction of osteoarthritis rats through the activation of the Janus kinase/signal transducers and activators of transcription signaling pathway by upregulating IFNA1

Yang

Zhang

Qian

et al. 2018

Journal Cellular Physiology

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Osteoarthritis (OA) is the most common disease of arthritis, a chronic joint disease that is always correlated with massive destruction such as cartilage destruction, inflammation of the synovial membrane, and so on. This study aims to explore the role of long noncoding RNA (lncRNA) LOC101928134 in the synovial hyperplasia and cartilage destruction, more specifically, in the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway in an OA rat model. Microarray‐based gene expression analysis was conducted to screen out the lncRNA differentially expressed in OA and predict the target gene of the lncRNA with the involvement of the signaling pathway through Kyoto encyclopedia of genes and genomes (KEGG) analysis. A model of OA was established and treated with the small interfering RNA LOC101928134/inhibitor of JAK/STAT signaling pathway to investigate the relationship among LOC101928134, IFNA1, and the JAK/STAT signaling pathway in OA. The effect of LOC101928134 on the serum levels of IFNA1, interleukin‐1β, and tumor necrosis factor‐α, and the apoptosis of synovial and cartilage cells was evaluated. LOC101928134, which was found to be highly expressed in knee joint synovial tissues of OA rats, regulated the expression of IFNA1 gene and inhibited JAK/STAT signaling pathway. Downregulation of LOC101928134 resulted in reduced knee joint synovitis, relived inflammatory damage, and knee joint cartilage damage of OA rats. Besides, synovial cell apoptosis was enhanced upon LOC101928134 downregulation, while cartilage cell apoptosis of OA rats was suppressed. These results demonstrate that downregulation of LOC101928134 suppresses the synovial hyperplasia and cartilage destruction of OA rats via activation of JAK/STAT signaling pathway by upregulating IFNA1, providing a new candidate for the treatment of OA.

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Section: Discussionmentioning

confidence: 99%

Downregulation of long noncoding RNA LOC101928134 inhibits the synovial hyperplasia and cartilage destruction of osteoarthritis rats through the activation of the Janus kinase/signal transducers and activators of transcription signaling pathway by upregulating IFNA1

Yang

Zhang

Qian

et al. 2018

Journal Cellular Physiology

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“…We also shed light on the controversial question about the impact of these promoter polymorphisms on the expression of IFNAR-1 gene. The expression levels of the receptor are associated with the clinical outcome of chronically HBV-infected patients ( 49 ). We conclude that the expression of the major IFNAR-1 transcript, which is responsible for the production of the functional receptor, is not significantly affected by these polymorphisms (Figure 2 ).…”

Section: Discussionmentioning

confidence: 99%

Impact of Interferon-α Receptor-1 Promoter Polymorphisms on the Transcriptome of the Hepatitis B Virus-Associated Hepatocellular Carcinoma

et al. 2018

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Background and aimsGenetic polymorphisms within the promoter of interferon-α receptor type-1 (IFNAR1) have been associated with the susceptibility to and the outcome of chronic hepatitis B virus (HBV) infection. However, the impact of these polymorphisms in the transcriptome of the HBV-associated hepatocellular carcinoma (HCC) remains largely unexplored.MethodsUsing whole-genome and exome sequencing data from The Cancer Genome Atlas project, we characterized three single-nucleotide polymorphisms (SNPs: −568G/C, −408C/T, −3C/T) and one variable number tandem repeat [VNTR: −77(GT)n] within the IFNAR1 promoter sequence in 49 HCC patients. RNAseq data from 10 genotyped HCC samples were grouped according to their −77VNTR or −3SNP genotype to evaluate the impact of these polymorphisms on the differential expression on the HCC transcriptome.ResultsThere is a fourfold higher impact of the −77VNTR on the HCC transcriptome compared to the −3SNP (q < 0.1, p < 0.001). The expression of the primary IFNAR1 transcript is not affected by these polymorphisms but a secondary, HCC-specific transcript is expressed only in homozygous −77VNTR ≤8/≤8(GT)n samples (p < 0.05). At the same time, patients carrying at least one −77VNTR >8(GT) allele, presented a strong upregulation of the fibronectin-1 (FN-1) gene, which has been associated with the development of HCC. Gene Ontology and pathway enrichment analysis of the differentially expressed genes revealed a strong disruption of the PI3K–AKT signaling pathway, which can be partially triggered by the extracellular matrix FN-1.ConclusionThe IFNAR-1 promoter polymorphisms are not involved in the expression levels of the main IFNAR-1 transcript. The −77VNTR has a regulatory role on the expression of a secondary, truncated, HCC-specific transcript, which in turn coincides with disruptions in cancer-associated pathways and in FN-1 expression modifications.

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“…In addition, the dysregulated IFN responses are indicative of the successful immunomodulatory strategies used by beta coronaviruses [10]. Chronic HBV infection is related with the polymorphic IFNA1 (−2) gene variation, and in these individuals, the pathogenesis of chronic infection may be influenced by the differential expression of the IFNAR1 and IFNA1 genes [11].…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphism of IFNA1 and IFNAR1 Genes in Covid-19 Iraqi Patients

Almukhtar¹,

Ali²,

A.Mahmood³

2023

ANJS

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Coronavirus disease 2019 (Covid-19) is a deadly acute respiratory illness brought on by an infection with coronavirus 2. (SARS-CoV-2).The severity of the syndrome was variant among the individuals ranging between severe and mild. Interferons type 1 are one of the cytokines inactive the viral replication. Genetic variation inrs2850015 for IFNA1 and rs202055606 for IFNAR1 were investigated by high-resolution melting analysis. Results showed that TT genotype and T allele of rs20205560 6polymorphism represented a significant positive odds ratio as risk factor for severity while C allele act as protective factor. The rs2850015 polymor phismrevealed conversionT to G,the GG genotype and G allele represented a significant positive odds ratio as risk factor for severity while the T allele represent protective factorfrom severity. It wasbe concluded that the GG geno type and G allele for rs2850015 and TT genotype and T allelemay be associated with severity of Covid-19

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Association between the <b><i>IFNA1 </i></b>(-2C→T) Polymorphism and Increased <b><i>IFNAR1 </i></b>Gene Expression Levels in Chronic Hepatitis B Infection

Cited by 3 publications

References 36 publications

Downregulation of long noncoding RNA LOC101928134 inhibits the synovial hyperplasia and cartilage destruction of osteoarthritis rats through the activation of the Janus kinase/signal transducers and activators of transcription signaling pathway by upregulating IFNA1

Downregulation of long noncoding RNA LOC101928134 inhibits the synovial hyperplasia and cartilage destruction of osteoarthritis rats through the activation of the Janus kinase/signal transducers and activators of transcription signaling pathway by upregulating IFNA1

Impact of Interferon-α Receptor-1 Promoter Polymorphisms on the Transcriptome of the Hepatitis B Virus-Associated Hepatocellular Carcinoma

Genetic Polymorphism of IFNA1 and IFNAR1 Genes in Covid-19 Iraqi Patients

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