Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA

Liu, Xiaoyun; Jiao, Yan; Cao, Yukun; Deng, Nan; Ma, Yuru; Hasty, Karen A.; Kang, Andrew H.; Chen, Hong; Stuart, J.; Gu, Weikuan

doi:10.1186/s12865-016-0163-y

Cited by 7 publications

(4 citation statements)

References 47 publications

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“…Lefty1 encodes a secreted ligand of the TGF-beta superfamily of proteins 43 . A gene expression comparison between the congenic Bagg Albinos D1-1 (BALB.D1-1) mice and the parental BALB/c À/strain revealed that Lefty1 was down-regulated in the congenic strain in joint tissue, which is relatively resistant to spontaneous arthritis 44 .…”

Section: Osteoarthritis Andcartilagementioning

confidence: 99%

RNA-seq analysis of chondrocyte transcriptome reveals genetic heterogeneity in LG/J and SM/J murine strains

Duan

Cai

Schmidt

et al. 2020

Osteoarthritis and Cartilage

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Objective: To investigate the transcriptomic differences in chondrocytes obtained from LG/J (large, healer) and SM/J (small, non-healer) murine strains in an attempt to discern the molecular pathways implicated in cartilage regeneration and susceptibility to osteoarthritis (OA). Design: We performed RNA-sequencing on chondrocytes derived from LG/J (n ¼ 16) and SM/J (n ¼ 16) mice. We validated the expression of candidate genes and compared single nucleotide polymorphisms (SNPs) between the two mouse strains. We also examined gene expression of positional candidates for ear pinna regeneration and long bone length quantitative trait loci (QTLs) that display differences in cartilaginous expression. Results: We observed a distinct genetic heterogeneity between cells derived from LG/J and SM/J mouse strains. We found that gene ontologies representing cell development, cartilage condensation, and regulation of cell differentiation were enriched in LG/J chondrocytes. In contrast, gene ontologies enriched in the SM/J chondrocytes were mainly related to inflammation and degeneration. Moreover, SNP analysis revealed that multiple validated genes vary in sequence between LG/J and SM/J in coding and highly conserved noncoding regions. Finally, we showed that most QTLs have 20e30% of their positional candidates displaying differential expression between the two mouse strains. Conclusions: While the enrichment of pathways related to cell differentiation, cartilage development and cartilage condensation infers superior healing potential of LG/J strain, the enrichment of pathways related to cytokine production, immune cell activation and inflammation entails greater susceptibility of SM/J strain to OA. These data provide novel insights into chondrocyte transcriptome and aid in identification of the quantitative trait genes and molecular differences underlying the phenotypic differences associated with individual QTLs.

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Section: Osteoarthritis Andcartilagementioning

confidence: 99%

RNA-seq analysis of chondrocyte transcriptome reveals genetic heterogeneity in LG/J and SM/J murine strains

Duan

Cai

Schmidt

et al. 2020

Osteoarthritis and Cartilage

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“…By focusing on transcription factors with putative relevance to the polarization of monocytes towards classically activated M1 or alternatively activated M2 macrophages, we found that during infection with L. monocytogenes , the activation and development of proinflammatory monocytes is characterized by factors, such as Irf1, Irf2, Ifi204, Batf2, Mndal, and Irf7 [ 24 , 25 , 26 , 27 , 28 ] ( Figure 3 A). By contrast, during E. histolytica infection, Ly6C hi monocytes are characterized by the upregulation of transcription factors Mafb, Hes1, Fos, and Tsc22d3 ( Figure 3 A), which contribute to an anti-inflammatory and regenerative phenotype [ 29 , 30 , 31 , 32 , 33 ].…”

Section: Resultsmentioning

confidence: 99%

“…However, some genes were differentially regulated, e.g., Arg1/Arg 2 , further suggesting an ongoing polarization into an anti-inflammatory M2 phenotype. In contrast, monocytes from the L. monocytogenes infection model were characterized by a classical proinflammatory, interferon-driven transcription factor-like profile (i.e., Mndal , Ifi204 and Irf2 ) [ 25 , 28 ], pointing towards an M1 phenotype [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

The Properties of Proinflammatory Ly6Chi Monocytes Are Differentially Shaped by Parasitic and Bacterial Liver Infections

Hoenow

Yan

Noll

et al. 2022

Cells

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In the past, proinflammatory CD11b+Ly6Chi monocytes were predominantly considered as a uniform population. However, recent investigations suggests that this population is far more diverse than previously thought. For example, in mouse models of Entamoeba (E.) histolytica and Listeria (L.) monocytogenes liver infections, it was shown that their absence had opposite effects. In the former model, it ameliorated parasite-dependent liver injury, whereas in the listeria model it exacerbated liver pathology. Here, we analyzed Ly6Chi monocytes from the liver of both infection models at transcriptome, protein, and functional levels. Paralleled by E. histolytica- and L. monocytogenes-specific differences in recruitment-relevant chemokines, both infections induced accumulation of Ly6C+ monocytes at infection sites. Transcriptomic analysis revealed a high similarity between monocytes from naïve and parasite-infected mice and a clear proinflammatory phenotype of listeria-induced monocytes. This was further reflected by the upregulation of M2-related transcription factors (e.g., Mafb, Nr4a1, Fos) and higher CD14 expression by Ly6Chi monocytes in the E. histolytica infection model. In contrast, monocytes from the listeria infection model expressed M1-related transcription factors (e.g., Irf2, Mndal, Ifi204) and showed higher expression of CD38, CD74, and CD86, as well as higher ROS production. Taken together, proinflammatory Ly6Chi monocytes vary considerably depending on the causative pathogen. By using markers identified in the study, Ly6Chi monocytes can be further subdivided into different populations.

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“…In their report, Alunno et al showed that high levels of circulating IFI16 in RA are more frequent in RF/anti-CCP-positive RA patients and significantly associated with pulmonary involvement. Most recently, a study using the IL-1RA-deficient mouse model found that decreased expression levels of Ifi genes were associated with increased resistance to SAD [ 10 ]. In addition, previously, interferon-inducible protein-10 (IP-10) was found to be linked to RA, although it is not located in the human HIN-200 cluster [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Correlation with Gene Expression Levels between Ifi200 Family Genes and Four Sets of Immune Disease-Relevant Genes

Cao

Wang

et al. 2018

Journal of Immunology Research

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Background The HIN-200 family genes in humans have been linked to several autoimmune diseases—particularly to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Recently, its human counterpart gene cluster, the Ifi200 family in mice, has been linked to spontaneous arthritis disease (SAD). However, many immune-mediated diseases (including RA and SLE) show gender difference. Understanding whether or not and how these genes play a role in sex difference in immune-mediated diseases is essential for diagnosis/treatment. Methods This study takes advantage of the whole genome gene expression profiles of recombinant inbred (RI) strain populations from female and male mice to analyze potential sex differences in a variety of genes in disease pathways. Expression levels and regulatory QTL of Ifi200 family genes between female and male mice were first examined in a large mouse population, including RI strains derived from C57BL/6J, DBA/2J (BXD), and classic inbred strains. Sex similarities and differences were then analyzed for correlations with gene expression levels between genes in the Ifi200 family and four selected gene sets: known immune Ifi200 pathway-related genes, lupus-relevant genes, osteoarthritis- (OA-) and RA-relevant genes, and sex hormone-related genes. Results The expression level of Ifi202b showed the most sex difference in correlation with known immune-related genes (the P value for Ifi202b is 0.0004). Ifi202b also showed gender difference in correlation with selected sex hormone genes, with a P value of 0.0243. When comparing coexpression levels between Ifi200 genes and lupus-relevant genes, Ifi203 and Ifi205 showed significant sex difference (P values: 0.0303 and 0.002, resp.). Furthermore, several key genes (e.g., Csf1r, Ifnb1, IL-20, IL-22, IL-24, Jhdm1d, Csf1r, Ifnb1, IL-20, IL-22, IL-24, and Tgfb2 that regulate sex differences in immune diseases) were discovered. Conclusions Different genes in the Ifi200 family play different roles in sex difference among dissimilar pathways of these four gene groups.

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Decreased expression levels of Ifi genes is associated to the increased resistance to spontaneous arthritis disease in mice deficiency of IL-1RA

Cited by 7 publications

References 47 publications

RNA-seq analysis of chondrocyte transcriptome reveals genetic heterogeneity in LG/J and SM/J murine strains

RNA-seq analysis of chondrocyte transcriptome reveals genetic heterogeneity in LG/J and SM/J murine strains

The Properties of Proinflammatory Ly6Chi Monocytes Are Differentially Shaped by Parasitic and Bacterial Liver Infections

Sex Differences in Correlation with Gene Expression Levels between Ifi200 Family Genes and Four Sets of Immune Disease-Relevant Genes

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