Upregulated renal tubular CD44, hyaluronan, and osteopontin in kdkd mice with interstitial nephritis

Sibalic, Vladimir; Fan, Xiaohong; Loffing, Johannes; Wüthrich, Rudolf P.

doi:10.1093/ndt/12.7.1344

Cited by 87 publications

(75 citation statements)

References 12 publications

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“…In autoimmune disease-prone MRL/lpr mice, the level of OPN in serum was found to be increased in association with the onset of autoimmune diseases and expansion of CD3 + /CD4 -/CD8 -T-cells which express OPN mRNA [16]. Several studies have demonstrated the link between OPN overexpression and autoimmune diseases including lupus nephritis [28,29], interstitial nephritis [30], rheumatoid arthritis [31] and pulmonary fibrosis [32]. These findings suggest that there is a quantitative contribution of OPN activity to autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Implication of allelic polymorphism of osteopontin in the development of lupus nephritis in MRL/lpr mice

Miyazaki

Ono

et al. 2005

Eur J Immunol

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Potentially, autoimmune diseases develop from a combination of multiple genes with allelic polymorphisms. An MRL/Mp-Fas lpr/lpr (MRL/lpr) strain of mice develops autoimmune diseases, including lupus nephritis, but another lpr strain, C3H/HeJFas lpr/lpr (C3H/lpr) does not. This indicates that MRL polymorphic genes are involved in the development of the diseases. By quantitative trait loci (QTL) analysis using 527 of the (MRL/lpr Â C3H/lpr)F 2 mice, we identified a novel locus for susceptibility to lupus nephritis at map position D5Mit115 on chromosome 5, the same alias of the osteopontin (Opn) gene (LOD score =4.0), susceptible in the MRL allele. In functional analyses of the MRL and C3H Opn alleles using synthetic osteopontin (OPN) made with a new method "cell-free system" with wheat germ ribosomes, the MRL-OPN induced higher expression and production of immunoglobulins as well as cytokines including TNF-a, IL-1b and IFN-c in splenocytes and/or macrophages than that of the C3H allele. These findings suggest that allelic polymorphism of OPN causes the functional differences in antibody production and macrophage activation between MRL and C3H strains, possibly involved in the development of lupus nephritis.

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Section: Discussionmentioning

confidence: 99%

Implication of allelic polymorphism of osteopontin in the development of lupus nephritis in MRL/lpr mice

Miyazaki

Ono

et al. 2005

Eur J Immunol

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“…The resulting cDNA (0.5 µl) was subjected to PCR with the primers shown in Table I. Eight of the primer sequences were derived from previously published ones, [19][20][21][22] while the others were designed from DDBJ sequences (DNA Database of Japan, Mishima, http://www.ddbj.nig.ac.jp/) with OLIGO Primer Analysis Software (National Biosciences, Plymouth, MN). The templates without reverse transcription were also prepared to evaluate contamination with genomic DNA.…”

Section: Methodsmentioning

confidence: 99%

A Murine Osteosarcoma Cell Line with a Potential to Develop Ossification upon Transplantation

Kusumi¹,

Nishi²,

Tanaka³

et al. 2001

Japanese Journal of Cancer Research

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An osteosarcoma cell line has been established from a soft tissue tumor that occurred spontaneously in a BALB/c mouse. This cell line showed ossification when transplanted into syngeneic mice. To examine the mechanism of bone formation, the expression of mRNAs for osteoblastic and chondroblastic markers and factors associated with ossification has been investigated. In culture, the cells exhibited a spindle shape in the growth phase, but had a polygonal shape in the stationary phase. Reverse transcription-polymerase chain reaction analysis showed that the cells expressed mRNAs for pro-α α α α1 (

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“…After being washed three times, various numbers of DCs were cultured together with 1 × 10 5 OT-I CD8 + T cells/well in U-bottomed 96-well plates. Cells were pulsed with 5 μCi/well of [ 3 H]thymidine on day 3 (1 μCi/well for peptide presentation) and then were collected [17][18][19][20][21][22][23][24] h later. T cell proliferation was evaluated by incorporation of [ 3 H]thymidine from triplicate wells.…”

Section: In Vitro Cross-presentation Assaymentioning

confidence: 99%

“…Opn is expressed in activated T cells, DCs and macrophages within 24 h of viral or bacterial infection and may account for resistance to microbial infection 13,16 . Dysregulated expression of Opn, in contrast, has been associated with autoimmune disease in mouse models 14 and in several types of human autoimmune disorders, including lupus nephritis, multiple sclerosis and rheumatoid arthritis [17][18][19][20][21][22] . Although most studies have focused on the activity of secreted Opn as a cytokine or chemokine 14,15,23 , a portion of newly synthesized Opn is retained as intracellular Opn (Opn-i) in the cytoplasm and distinct from secretory vesicles [24][25][26] .…”

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confidence: 99%

Osteopontin expression is essential for interferon-α production by plasmacytoid dendritic cells

et al. 2006

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The observation that the T-bet transcription factor allows tissue-specific upregulation of intracellular osteopontin (Opn-i) in plasmacytoid dendritic cells (pDCs) suggests that Opn might contribute to the expression of interferon-α (IFN-α) in those cells. Here we show that Opn deficiency substantially reduced Toll-like receptor 9 (TLR9)-dependent IFN-α responses but spared expression of transcription factor NF-κB-dependent proinflammatory cytokines. Shortly after TLR9 engagement, colocalization of Opn-i and the adaptor molecule MyD88 was associated with induction of transcription factor IRF7-dependent IFN-α gene expression, whereas deficient expression of Opn-i was associated with defective nuclear translocation of IRF7 in pDCs. The importance of the Opn-IFN-α pathway was emphasized by its essential involvement in crosspresentation in vitro and in anti-herpes simplex virus 1 IFN-α response in vivo. The finding that Opn-i selectively coupled TLR9 signaling to expression of IFN-α but not to that of other proinflammatory cytokines provides new molecular insight into the biology of pDCs.Increasing evidence that innate immune responses can determine both the type and intensity of adaptive immune responses has stimulated great interest in the underlying regulatory mechanisms. The recognition phase of innate responses depends on a series of patternrecognition receptors, including Toll-like receptors (TLRs) expressed by dendritic cells (DCs), which detect a wide range of pathogen-associated molecules carried by bacteria and viruses 1 . Engagement of the TLR9 family of endosomal receptors by microbe-derived DNA triggers the production of large amounts of interferons α and β (IFN-αβ) 2 , key mediators that regulate the development of both innate and adaptive immunity [3][4][5][6] . However, the pathway initiated by TLR9 engagement that culminates in IFN-αβ production is not fully understood.

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Upregulated renal tubular CD44, hyaluronan, and osteopontin in kdkd mice with interstitial nephritis

Cited by 87 publications

References 12 publications

Implication of allelic polymorphism of osteopontin in the development of lupus nephritis in MRL/lpr mice

Implication of allelic polymorphism of osteopontin in the development of lupus nephritis in MRL/lpr mice

A Murine Osteosarcoma Cell Line with a Potential to Develop Ossification upon Transplantation

Osteopontin expression is essential for interferon-α production by plasmacytoid dendritic cells

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