Ifi204 as the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra

Cheng Tian, Xiaoyun Liu, Xiaodong Zhu, Yanhong Cao, Nan Deng, Karen Hasty, John M. Stuart, Weikuan Gu, Yan Jiao

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Abstract

Aims: To examine whether the increased expression level of interferon-activatable protein (Ifi) genes is associated with the decreased resistance to SAD in a congenic mouse strain DBA.B-1−/− which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a BALB/c−/− on the DBA/1−/− background. Methods: We produced whole genome expression profiles from the DBA.B-1−/− and four parental strains, the wild type BALB/c, DBA/1 and the IL1rn-deficient DBA/1−/− and BALB/c−/−. We analyzed the differential expression levels of genes in DBA.B-1−/− in comparison to other strains, compared these genes with that of a previous congenic strain, BALB.D1-1−/−, which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a DBA/1−/− on the BALB/c−/− background and examined the candidacy of genes within the Ifi family. Results: Although there are a considerable number of differentially expressed genes between DBA.B-1−/− and the four parental strains, the differences are in the opposite direction to that in previous comparisons between the BALB.D1-1−/− and other strains. There were a fewer number of up-regulated genes in BALB.D1-1−/− in comparison to DBA/1. Instead of down-regulated Ifi genes in BALB.D1-1−/− in comparison to its parental strain BALB/c−/−, the expression levels of a few Ifi genes in the DBA.B-1−/− strain were higher than that of its parental strain DBA/1−/−. These Ifi genes are also differentially expressed between DBA.B-1−/− and DBA/1 strains. Their expression levels in the DBA.B-1−/− are similar to that in BALB/c and BALB/c−/− strains. Among these genes, only Ifi204 expressed at a significant, high level in these mouse strains. Conclusion: Ifi204 is the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. Both Htra1 and Dpt may be involved in the Ifi204 molecular pathway.

Original languageEnglish (US)
Pages (from-to)21-29
Number of pages9
JournalGene Reports
Volume12
DOIs
StatePublished - Sep 1 2018

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Interleukin 1 Receptor Antagonist Protein
Arthritis
Genes
Congenic Mice
Interferons
Genome
Gene Expression

All Science Journal Classification (ASJC) codes

  • Genetics

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Ifi204 as the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. / Tian, Cheng; Liu, Xiaoyun; Zhu, Xiaodong; Cao, Yanhong; Deng, Nan; Hasty, Karen; Stuart, John M.; Gu, Weikuan; Jiao, Yan.

In: Gene Reports, Vol. 12, 01.09.2018, p. 21-29.

Research output: Contribution to journalArticle

Tian, Cheng ; Liu, Xiaoyun ; Zhu, Xiaodong ; Cao, Yanhong ; Deng, Nan ; Hasty, Karen ; Stuart, John M. ; Gu, Weikuan ; Jiao, Yan. / Ifi204 as the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. In: Gene Reports. 2018 ; Vol. 12. pp. 21-29.
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abstract = "Aims: To examine whether the increased expression level of interferon-activatable protein (Ifi) genes is associated with the decreased resistance to SAD in a congenic mouse strain DBA.B-1−/− which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a BALB/c−/− on the DBA/1−/− background. Methods: We produced whole genome expression profiles from the DBA.B-1−/− and four parental strains, the wild type BALB/c, DBA/1 and the IL1rn-deficient DBA/1−/− and BALB/c−/−. We analyzed the differential expression levels of genes in DBA.B-1−/− in comparison to other strains, compared these genes with that of a previous congenic strain, BALB.D1-1−/−, which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a DBA/1−/− on the BALB/c−/− background and examined the candidacy of genes within the Ifi family. Results: Although there are a considerable number of differentially expressed genes between DBA.B-1−/− and the four parental strains, the differences are in the opposite direction to that in previous comparisons between the BALB.D1-1−/− and other strains. There were a fewer number of up-regulated genes in BALB.D1-1−/− in comparison to DBA/1. Instead of down-regulated Ifi genes in BALB.D1-1−/− in comparison to its parental strain BALB/c−/−, the expression levels of a few Ifi genes in the DBA.B-1−/− strain were higher than that of its parental strain DBA/1−/−. These Ifi genes are also differentially expressed between DBA.B-1−/− and DBA/1 strains. Their expression levels in the DBA.B-1−/− are similar to that in BALB/c and BALB/c−/− strains. Among these genes, only Ifi204 expressed at a significant, high level in these mouse strains. Conclusion: Ifi204 is the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. Both Htra1 and Dpt may be involved in the Ifi204 molecular pathway.",
author = "Cheng Tian and Xiaoyun Liu and Xiaodong Zhu and Yanhong Cao and Nan Deng and Karen Hasty and Stuart, {John M.} and Weikuan Gu and Yan Jiao",
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T1 - Ifi204 as the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra

AU - Tian, Cheng

AU - Liu, Xiaoyun

AU - Zhu, Xiaodong

AU - Cao, Yanhong

AU - Deng, Nan

AU - Hasty, Karen

AU - Stuart, John M.

AU - Gu, Weikuan

AU - Jiao, Yan

PY - 2018/9/1

Y1 - 2018/9/1

N2 - Aims: To examine whether the increased expression level of interferon-activatable protein (Ifi) genes is associated with the decreased resistance to SAD in a congenic mouse strain DBA.B-1−/− which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a BALB/c−/− on the DBA/1−/− background. Methods: We produced whole genome expression profiles from the DBA.B-1−/− and four parental strains, the wild type BALB/c, DBA/1 and the IL1rn-deficient DBA/1−/− and BALB/c−/−. We analyzed the differential expression levels of genes in DBA.B-1−/− in comparison to other strains, compared these genes with that of a previous congenic strain, BALB.D1-1−/−, which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a DBA/1−/− on the BALB/c−/− background and examined the candidacy of genes within the Ifi family. Results: Although there are a considerable number of differentially expressed genes between DBA.B-1−/− and the four parental strains, the differences are in the opposite direction to that in previous comparisons between the BALB.D1-1−/− and other strains. There were a fewer number of up-regulated genes in BALB.D1-1−/− in comparison to DBA/1. Instead of down-regulated Ifi genes in BALB.D1-1−/− in comparison to its parental strain BALB/c−/−, the expression levels of a few Ifi genes in the DBA.B-1−/− strain were higher than that of its parental strain DBA/1−/−. These Ifi genes are also differentially expressed between DBA.B-1−/− and DBA/1 strains. Their expression levels in the DBA.B-1−/− are similar to that in BALB/c and BALB/c−/− strains. Among these genes, only Ifi204 expressed at a significant, high level in these mouse strains. Conclusion: Ifi204 is the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. Both Htra1 and Dpt may be involved in the Ifi204 molecular pathway.

AB - Aims: To examine whether the increased expression level of interferon-activatable protein (Ifi) genes is associated with the decreased resistance to SAD in a congenic mouse strain DBA.B-1−/− which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a BALB/c−/− on the DBA/1−/− background. Methods: We produced whole genome expression profiles from the DBA.B-1−/− and four parental strains, the wild type BALB/c, DBA/1 and the IL1rn-deficient DBA/1−/− and BALB/c−/−. We analyzed the differential expression levels of genes in DBA.B-1−/− in comparison to other strains, compared these genes with that of a previous congenic strain, BALB.D1-1−/−, which is IL1rn-deficient and contains the QTL genomic fragment associated with susceptibility to SAD, from a DBA/1−/− on the BALB/c−/− background and examined the candidacy of genes within the Ifi family. Results: Although there are a considerable number of differentially expressed genes between DBA.B-1−/− and the four parental strains, the differences are in the opposite direction to that in previous comparisons between the BALB.D1-1−/− and other strains. There were a fewer number of up-regulated genes in BALB.D1-1−/− in comparison to DBA/1. Instead of down-regulated Ifi genes in BALB.D1-1−/− in comparison to its parental strain BALB/c−/−, the expression levels of a few Ifi genes in the DBA.B-1−/− strain were higher than that of its parental strain DBA/1−/−. These Ifi genes are also differentially expressed between DBA.B-1−/− and DBA/1 strains. Their expression levels in the DBA.B-1−/− are similar to that in BALB/c and BALB/c−/− strains. Among these genes, only Ifi204 expressed at a significant, high level in these mouse strains. Conclusion: Ifi204 is the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra. Both Htra1 and Dpt may be involved in the Ifi204 molecular pathway.

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