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| 1 | Inhibition of smoothened decreases proliferation of Synoviocytes in rheumatoid arthritis显示文摘像成纤维细胞的 synoviocytes (FLS ) 在风湿性关节炎(RA ) 贡献 synovial 增生。Smoothened (Smo ) 是发信号的声音的刺猬(嘘) 的一个关键部件并且贡献肿瘤房间增长。这研究的目的是在 RA synoviocyte 增长调查 Smo 的角色。FLS 从 RA synovium 被孤立。发信号的嘘用一个 Smo 对手(GDC-0449 ) 和在 FLS 指向 Smo 基因的小介入 RNA (siRNA ) 被学习。房间增长被使用 kit-8 试金和房间周期分发确定, apoptosis 被流动 cytometry 评估。房间周期相关的基因和蛋白质被即时 PCR 和西方的污点检测。与 GDC-0449 或 Smo-siRNA 对待的 FLS 与控制相比显示出显著地减少的增长(P < 0.05 ) 。有 GDC-0449 的孵化或有 Smo-siRNA 的 transfection 与控制相比导致了 G 1 阶段房间的重要增加(P < 0.05 ) 。房间周期拘捕被 cyclin D1 和 E1 mRNA 表示的重要增加验证,在在 Smo-siRNA transfected 房间的 cyclin 依赖的 kinase p21 mRNA 表示的减少(P < 0.05 ) 。cyclin D1 的蛋白质表示也是在 Smo 基因以后的 downregulated 击倒(P < 0.05 ) 。结果建议发信号的嘘以一种 Smo 依赖的方式在 RA-FLSs 增长起一个重要作用并且可以贡献 synovial 增生。指向嘘发信号可以帮助与 RA 在病人控制联合损坏。 | Shang-ling Zhu Jian-lin Huang Wei-xiang Peng Dan-chun Wu Min-qi Luo Qiu-xia Li Zhao-xia Li Xiao-xue Feng Fang Liu Ming-xia Wang Wei-qian Chen Nancy Olsen Song Guo Zheng | 2017 | Cellular & Molecular Immunology2017，14，2： | 9 |
| 2 | uPAR promotes tumor-like biologic behaviors of fibroblast-like synoviocytes through PI3K/Akt signaling pathway in patients with rheumatoid arthritis显示文摘Urokinase-type plasminogen activator receptor(uPAR),is a multifunctional receptor on cell surface,widely present in endothelial cells,fibroblasts,and a variety of malignant cells.Current studies have suggested that uPAR overexpressed on synovial tissues or in synovial fluid or plasma in patients with rheumatoid arthritis(RA).However,there are limited researches regarding the role of uPAR on fibroblast-like synoviocytes of rheumatoid arthritis(RA-FLSs)and its underlying mechanisms.Here,our studies show that the expression of uPAR protein was significantly higher in fibroblast-like synoviocytes(FLSs)from RA than those from osteoarthritis or traumatic injury patients.uPAR gene silencing significantly inhibited RA-FLSs cell proliferation,restrained cell transformation from the G0/G1 phase to S phase,aggravated cell apoptosis,interfered with RA-FLSs cell migration and invasion,and reduced activation of the PI3K/Akt signaling pathway,which may be associated withβ1-integrin.Cell supernatants from uPAR gene-silenced RA-FLSs markedly inhibited the migration and tubule formation ability of the HUVECs(a human endothelial cell line).Therefore,we demonstrate that uPAR changes the biological characteristics of RA-FLSs,and affects neoangiogenesis of synovial tissues in patients with RA.All of these may be associated with theβ1-integrin/PI3K/Akt signaling pathway.These results imply that targeting uPAR and its downstream signal pathway may provide therapeutic effects in RA. | Yan Liu Yun Feng Pan You-qiu Xue Lin-kai Fang Xing-hua Guo Xin Guo Meng Liu Bi-yao Mo Meng-ru Yang Fang Liu Yun-ting Wu Nancy Olsen Song Guo Zheng | 2018 | Cellular & Molecular Immunology2018，15，2： | 9 |
| 3 | High salt diet accelerates the progression of murine lupus through dendritic cells via the p38 MAPK and STAT1 signaling pathways显示文摘The increased incidence of systemic lupus erythematosus(SLE)in recent decades might be related to changes in modern dietary habits.Since sodium chloride(NaCl)promotes pathogenic T cell responses,we hypothesize that excessive salt intake contributes to the increased incidence of autoimmune diseases,including SLE.Given the importance of dendritic cells(DCs)in the pathogenesis of SLE,we explored the influence of an excessive sodium chloride diet on DCs in a murine SLE model.We used an induced lupus model in which bone marrow-derived dendritic cells(BMDCs)were incubated with activated lymphocyte-derived DNA(ALD-DNA)and transferred into C57BL/6 recipient mice.We observed that a high-salt diet(HSD)markedly exacerbated lupus progression,which was accompanied by increased DC activation.NaCl treatment also stimulated the maturation,activation and antigenpresenting ability of DCs in vitro.Pretreatment of BMDCs with NaCl also exacerbated BMDC-ALD-DNA-induced lupus.These mice had increased production of autoantibodies and proinflammatory cytokines,more pronounced splenomegaly and lymphadenopathy,and enhanced pathological renal lesions.The p38 MAPK–STAT1 pathway played an important role in NaClinduced DC immune activities.Taken together,our results demonstrate that HSD intake promotes immune activation of DCs through the p38 MAPK–STAT1 signaling pathway and exacerbates the features of SLE.Thus,changes in diet may provide a novel strategy for the prevention or amelioration of lupus or other autoimmune diseases. | Ze Xiu Xiao Xiaojiang Hu Ximei Zhang Zhigang Chen Julie Wang Ke Jin Feng Lin Cao Baoqing Sun Joseph A.Bellanti Nancy Olsen Song Guo Zheng | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 6 |
| 4 | TGF-β-induced CD4+FoxP3+regulatory T cell-derived extracellular vesicles modulate Notch1 signaling through miR-449a and prevent collagen-induced arthritis in a murine model显示文摘CD4^(+)FOXP3^(+)Treg cells are central to the maintenance of self-tolerance and can be defective in autoimmunity.In autoimmune rheumatic diseases,dysfunctional self-tolerance,is to a large extent,caused by insufficient Treg-cell activity.Although nTregs have therapeutic effects in vivo,their relative scarcity and slow rate of in vitro expansion hinder the application of nTreg therapy.It was previously reported that EVs contribute significantly to the suppressive function of FOXP3^(+)Treg cells.Considering that the stability and plasticity of nTregs remain major challenges in vivo,we established EVs derived from in vitro TGF-β-induced Treg cells(iTreg-EVs)and assessed their functions in a murine model of autoimmune arthritis.The results demonstrated that iTreg-EVs preferentially homed to the pathological joint and efficiently prevented the imbalance in Th17/Treg cells in arthritic mice.Furthermore,we found that miR-449a-5p mediated Notch1 expression modulation and that miR-449a-5p knockdown abolished the effects of iTreg-EVs on effector T cells and regulatory T cells in vitro and in vivo.Taken together,our results show that iTreg-EVs control the inflammatory responses of recipient T cells through miR-449a-5p-dependent modulation of Notch1 and ameliorate the development and severity of arthritis,which may provide a potential cell-free strategy based on manipulating iTreg-EVs to prevent autoimmune arthritis. | Jingrong Chen Feng Huang Yuluan Hou Xiaorong Lin Rongzhen Liang Xiaojiang Hu Jun Zhao Julie Wang Nancy Olsen Song Guo Zheng | 2021 | Cellular & Molecular Immunology2021，18，11： | 2 |
| 5 | Utility of magnetic resonance imaging in the evaluation of patients with inflammatory myopathies显示文摘 | Jane H. Park MD Nancy J. Olsen MD | 2001 | Current Rheumatology Reports2001，，4： | 1 |
| 6 | New drugs for rheumatoid arthritis 显示文摘 | Nancy J Olsen C Michael S | 2004 | N Engl J Med2004，350，： | 1 |
| 7 | Profiles of gene expression in human autoimmune disease显示文摘 | Thomas M. Aune Kevin Maas Joel Parker Jason H. Moore Nancy J. Olsen | 2004 | Cell Biochemistry and Biophysics2004，，2： | 1 |
| 8 | RPehseaarcshe ar t1icle,placebo-controlled,dose escalation trial of chicory root extract in patients with osteoarthritis of the hip or knee显示文摘 | Nancy J Olsen Valerie K Branch Geetha Jonnala | 2010 | BMC Musculoskeletal Disorders2010，11，： | 1 |
| 9 | Biomarkers for Primary Sjgren's Syndrome显示文摘Primary Sjo¨gren's syndrome(p SS) is a systemic autoimmune disease with exocrine gland dysfunction and multi-organ involvement. Recent progress in understanding the pathogenesis of p SS offers an opportunity to find new biomarkers for the diagnosis and assessment of disease activity. Screening noninvasive biomarkers from the saliva and tears has significant potential. The need for specific and sensitive biomarker candidates in p SS is significant. This review aims to summarize recent advances in the identification of biomarkers of Sjo¨gren syndrome, trying to identify reliable, sensitive, and specific biomarkers that can be used to guide treatment decisions. | Weiqian Chen Heng Cao Jin Lin Nancy Olsen Song Guo Zheng | 2015 | Genomics, Proteomics & Bioinformatics2015，13，4： | 1 |
| 10 | Immunochemical and flow cytometric analysis of androgen receptor expression in thymocytes显示文摘 | Susan M Viselli Nancy J Olsen Keith Shults | 1995 | Molecular and Cellular Endocrinology1995，109，： | 1 |
| 11 | Utility of magnetic resonance imaging in the evaluation of patients with inflammatory myopathies显示文摘 | Jane H. Park MD Nancy J. Olsen MD | 2001 | Current Rheumatology Reports2001，，4： | 1 |
| 12 | Effects of androgens on T and B lymphocyte development显示文摘 | Nancy J. Olsen MD William J. Kovacs | 2001 | Immunologic Research (-)2001，，2： | 1 |
| 13 | A protocol to develop T helper and Treg cells in vivo显示文摘An understanding of the development and function of T helper(Th)1,Th17 and regulatory T(Treg)cells is critical toward revealing pro-inflammatory immune responses,especially in autoimmune diseases.However,there is no standard protocol to monitor the development of these cells over time in vivo.This protocol details a method to generate Th1,Th17,and Treg cells in a T cell-induced colitis model in vivo and monitor their dynamic changes,which can be used for further investigations in their development from naive CD4+T cells in specific gene knockouts and background strains. | Weiqian Chen Zhenjian Xu Yongjiang Zheng Julie Wang Wenbin Qian Nancy Olsen David Brand Jin Lin Song Guo Zheng | 2017 | Cellular & Molecular Immunology2017，14，12： | 1 |
| 14 | Advances in the role of follicular T helper cells in graft versus host diseases显示文摘Graft versus host disease(GVHD)is a refractory complication of allogeneic hematopoietic stem cell transplantation for the treatment of malignant and non-malignant hematopoietic diseases.Inflammatory cascade responses and cellular immune reactions are the major factors underlying GVHD pathogenesis.Cells producing the cytokine,interleukin(IL)-21 are crucial players involved in injured tissues in GVHD patients.Besides T helper 17 cells,follicular T helper(Tfh)cells are a new source of IL-21 and play a vital role in GVHD pathogenesis.Tfh cell function is mostly regulated by T-follicular regulatory(Tfr)cells that are also located in the germinal center.This review highlights recent advances in the role of Tfh and Tfr cell function in GVHD pathogenesis.New insights are provided into the potential for clinical application in GVHD prevention and treatment. | Maogen Chen Xiaohong Lin Julie Wang Nancy Olsen Song Guo Zheng | 2017 | Liver Research2017，1，2： | 0 |
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