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  • 11
    In: Metabolomics, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2018-1)
    Type of Medium: Online Resource
    ISSN: 1573-3882 , 1573-3890
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2182289-X
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  • 12
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 22, No. 23 ( 2021-11-25), p. 12764-
    Abstract: Toll-like receptors (TLRs) play a major role in the innate immune system. Several studies have shown the regulatory effects of TLR-mediated pathways on immune and inflammatory diseases. Dysregulated functions of TLRs within the endosomal compartment, including TLR7/9 trafficking, may cause systemic lupus erythematosus (SLE). TLR signaling pathways are fine-tuned by Toll/interleukin-1 receptor (TIR) domain-containing adapters, leading to interferon (IFN)-α production. This study describes a TLR inhibitor peptide 1 (TIP1) that primarily suppresses the downstream signaling mediated by TIR domain-containing adapters in an animal model of lupus and patients with SLE. The expression of most downstream proteins of the TLR7/9/myeloid differentiation factor 88 (MyD88)/IFN regulatory factor 7 signaling was downregulated in major tissues such as the kidney, spleen, and lymph nodes of treated mice. Furthermore, the pathological analysis of the kidney tissue confirmed that TIP1 could improve inflammation in MRL/lpr mice. TIP1 treatment downregulated many downstream proteins associated with TLR signaling, such as MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor 6, and IFN-α, in the peripheral blood mononuclear cells of patients with SLE. In conclusion, our data suggest that TIP1 can serve as a potential candidate for the treatment of SLE.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2019364-6
    SSG: 12
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  • 13
    In: Journal of Bone and Mineral Research, Wiley, Vol. 27, No. 10 ( 2012-10), p. 2075-2084
    Type of Medium: Online Resource
    ISSN: 0884-0431
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2008867-X
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  • 14
    In: Journal of Bone and Mineral Research, Wiley, Vol. 26, No. 2 ( 2011-02), p. 341-350
    Abstract: In bone remodeling, various transcriptional factors are involved, and the deficiency or overexpression of some of these factors results in bone defects. Myeloid elf‐1‐like factor (MEF) is one of the Ets transcription factors that control the expression of genes that are critical for biologic processes such as cell proliferation, differentiation, and death. Previously, we reported that MEF promotes cell proliferation and functions as a negative regulator of osteogenic differentiation by interacting directly with Runx2 and suppressing its transcriptional activity. To investigate the in vivo function of MEF in bone formation and bone remodeling in vivo, we generated transgenic mice that overexpress MEF in osteoblasts under the control of the 2.3‐kb Col1α1 promoter, named Col1α1‐MEF. Femoral bone in Col1α1‐MEF transgenic mice exhibited low bone mass with fewer trabecular bones and thinner and less developed cortical bones. The mineralized volume fraction (BV/TV) and bone‐forming rate (BFR) were remarkably decreased to about 63% and 40%, respectively, in 6‐week‐old MEF transgenic mice compared with wild‐type mice. In addition, reduced bone mineral density was observed in lumbar vertebrae of Col1α1‐MEF transgenic mice. The number of TRACP + osteoclasts was increased in Col1α1‐MEF transgenic mice and MEF‐overexpressing MC3T3‐E1 cells. All these in vivo results suggest that MEF suppresses bone formation by osteoblasts and facilitates bone resorption by activating osteoclasts indirectly. © 2011 American Society for Bone and Mineral Research.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2011
    detail.hit.zdb_id: 2008867-X
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  • 15
    In: Journal of Bone and Mineral Research, Wiley, Vol. 24, No. 6 ( 2009-06), p. 1055-1065
    Abstract: Osterix (Osx) is essential for osteoblast differentiation and bone formation, because mice lacking Osx die within 1 h of birth with a complete absence of intramembranous and endochondral bone formation. Perinatal lethality caused by the disruption of the Osx gene prevents studies of the role of Osx in bones that are growing or already formed. Here, the function of Osx was examined in adult bones using the time‐ and site‐specific Cre/loxP system. Osx was inactivated in all osteoblasts by Col1a1‐Cre with the activity of Cre recombinase under the control of the 2.3‐kb collagen promoter. Even though no bone defects were observed in newborn mice, Osx inactivation with 2.3‐kb Col1a1‐Cre exhibited osteopenia phenotypes in growing mice. BMD and bone‐forming rate were decreased in lumbar vertebra, and the cortical bone of the long bones was thinner and more porous with reduced bone length. The trabecular bones were increased, but they were immature or premature. The expression of early marker genes for osteoblast differentiation such as Runx2, osteopontin, and alkaline phosphatase was markedly increased, but the late marker gene, osteocalcin, was decreased. However, no functional defects were found in osteoclasts. In summary, Osx inactivation in growing bones delayed osteoblast maturation, causing an accumulation of immature osteoblasts and reducing osteoblast function for bone formation, without apparent defects in bone resorption. These findings suggest a significant role of Osx in positively regulating osteoblast differentiation and bone formation in adult bone.
    Type of Medium: Online Resource
    ISSN: 0884-0431 , 1523-4681
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2008867-X
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  • 16
    In: European Journal of Clinical Investigation, Wiley
    Abstract: Seasonal variation and sunlight exposure can impact serum vitamin D levels, potentially influencing lupus symptoms. We investigated seasonal vitamin D levels and their correlation with clinical manifestations and disease activity in systemic lupus erythematosus (SLE). Methods Serum 25(OH) vitamin D3 (25(OH)D3) levels were categorised as deficient (25(OH)D3  〈  10 ng/mL), insufficient (10–30 ng/mL) and sufficiency ( 〉 30 ng/mL) in participants analysed in winter ( n  = 407) and summer ( n  = 377). Logistic regression analysis was performed to assess the impact of vitamin D levels on achieving a lupus low disease activity state (LLDAS), stratified by season. Results The mean serum 25(OH)D3 levels differed significantly between the winter and summer measurement groups (22.4 vs. 24.2 ng/mL; p  = .018). The prevalences of vitamin D deficiency, insufficiency and sufficiency in the winter group were 12.8%, 66.6% and 20.6%, respectively, compared with 4.5%, 67.9% and 27.6% in the summer group. Achieving LLDAS was highest in the vitamin D sufficiency group (winter: 56.6%, summer: 55%) and lowest in the vitamin D deficiency group (winter: 15.4%, summer: 13.6%), with significant differences (all p   〈  .001). Multivariate analysis identified SLE disease activity index ≤4, normal anti‐double‐stranded DNA and vitamin D sufficiency as significant factors for achieving LLDAS in both seasons. Conclusions Sufficient vitamin D levels are important for achieving LLDAS in patients with SLE during winter and summer. Therefore, physicians should pay attention to the adequacy of vitamin D levels and consider recommending vitamin D supplementation for patients with vitamin D insufficiency.
    Type of Medium: Online Resource
    ISSN: 0014-2972 , 1365-2362
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2004971-7
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  • 17
    Online Resource
    Online Resource
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-4-22)
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-4-22)
    Abstract: This study aimed to elucidate the potential of serum, urine, and saliva S100 calcium-binding protein A8 protein (S100A8) levels as biomarkers for systemic lupus erythematosus (SLE). Methods Serum, urine, and saliva samples were obtained from 249 patients with SLE from the Ajou lupus cohort and 52 age- and sex-matched healthy controls (HCs). The concentrations of S100A8 were quantified using an ELISA, and a receiver operating characteristic curve was used to analyze whether they may be used as biomarkers for diagnosing SLE. Results Among 249 SLE patients included in our study, the mean SLE disease activity index (SLEDAI)-2K was 7.16 ± 5.61, and the number of patients with lupus flare was 11. Patients with SLE showed a 2.7-fold increase in serum S100A8 levels compared with that in HCs (1,890.6 vs. 709 pg/ml, p & lt; 0.001). In urine and saliva, the average S100A8 levels were significantly higher in patients with SLE compared with those in HCs (urine, 2,029.4 vs. 1,096.7 pg/ml, p = 0.001; saliva, 290,496.3 vs. 47,742 pg/ml, p & lt; 0.001). For SLE diagnosis, the area under the receiver operating characteristic curve was 0.831 for serum S100A8 (95% CI, 0.765–0.897), 0.751 for urine S100A8 (95% CI, 0.648–0.854), and 0.729 for salivary S100A8 (95% CI, 0.646–0.812). Pearson’s correlation analysis showed that S100A8 in serum, urine, and saliva was significantly associated with the SLEDAI (r = 0.267, p & lt; 0.001; r = 0.274, p & lt; 0.001; and r = 0.629, p & lt; 0.001, respectively). Among the clinical manifestations, nephritis was the most influential factor related to SLE in the concentration of S100A8 in serum, urine, and saliva. Conclusion This is the first study to show that the expression of S100A8 in serum, urine, and saliva is significantly higher in patients with SLE than in HCs and is associated with disease activity markers. Therefore, we suggest that S100A8 protein could be a potential biomarker for SLE.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 18
    Online Resource
    Online Resource
    Korean College of Rheumatology ; 2023
    In:  Journal of Rheumatic Diseases Vol. 30, No. 3 ( 2023-07-01), p. 198-203
    In: Journal of Rheumatic Diseases, Korean College of Rheumatology, Vol. 30, No. 3 ( 2023-07-01), p. 198-203
    Type of Medium: Online Resource
    ISSN: 2093-940X , 2233-4718
    Language: English
    Publisher: Korean College of Rheumatology
    Publication Date: 2023
    detail.hit.zdb_id: 3117751-7
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  • 19
    In: Bone, Elsevier BV, Vol. 46, No. 4 ( 2010-04), p. 920-928
    Type of Medium: Online Resource
    ISSN: 8756-3282
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2010
    detail.hit.zdb_id: 1496324-3
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  • 20
    In: Mediators of Inflammation, Hindawi Limited, Vol. 2019 ( 2019-02-28), p. 1-12
    Abstract: Liver X receptors (LXRs) have emerged as important regulators of inflammatory gene expression. Previously, we had reported that an LXR α gene promoter polymorphism (-1830 T  〉  C) is associated with systemic lupus erythematosus (SLE). Therefore, we assessed cytokine expression in relation to LXR α polymorphism in monocyte-derived macrophages from patients with SLE. Macrophages were obtained after 72 hours of culture of human monocytes supplemented with phorbol 12-myristate 13-acetate. Cells were transfected with LXR α promoter constructs. Additionally, peripheral blood mononuclear cell- (PBMC-) derived macrophages from the patients were evaluated for proinflammatory cytokines in relation to the genotypes of LXR α -1830 T  〉  C. The expression of LXR α was increased in macrophages; levels of proinflammatory cytokines were decreased with LXR α expression. Production of proinflammatory cytokines varied depending on LXR α -1830 T  〉  C genotype. In particular, expression of LXR α was decreased and that of proinflammatory cytokines was increased for LXR α -1830 TC genotype compared to that for TT genotype. The data were consistent in PBMC-derived macrophages from patients with SLE. Increased proinflammatory cytokines is related to TLR7 and TLR9 expression. These data suggest that the expression levels of LXR α , according to LXR α -1830 T  〉  C genotype, may contribute to the inflammatory response by induction of inflammatory cytokines in SLE.
    Type of Medium: Online Resource
    ISSN: 0962-9351 , 1466-1861
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2008065-7
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