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| 1 | Intracellular HMGB1 as a novel tumor suppressor of pancreatic cancer显示文摘尽管有最近的进展, oncogenic K 地岬驾驶的胰腺的 ductal 腺癌(PDAC ) 在最致命的人的癌症之中留在现代医学。PDAC 的致病对内在的染色体不稳定性和外来的发炎激活部分可归因。然而,在在胰腺的 tumorigenesis 的这二个事件之间的分子的连接充分还没被建立了。这里,我们证明(HMGB1 ) 细胞内部的高活动性组盒子 1 显著地压制 oncogenic 由禁止染色体的 K-Ras-driven 胰腺的 tumorigenesis 调停不稳定性的支持 inflammatory nucleosome 版本。任何一个单身者的有条件的基因脱离或在胰的 HMGB1 的两等位基因在出生使老鼠变为极其敏感到先锋损害的 oncogenic K-Ras-driven 开始,包括胰腺的 intraepithelial 瘤, intraductal 乳突的 mucinous 瘤,和 mucinous 膀胱的瘤。在胰的 HMGB1 的损失与染色体重新整理和 telomere 畸形描绘的氧化 DNA 损坏和 chromosomal 不稳定性被联系。这些导致煽动性的 nucleosome 版本并且宣传 K-Ras-driven 胰腺的 tumorigenesis。细胞外的 nucleosomes 支持 interleukin 6 (IL-6 ) 由渗入 macrophages/neutrophils 的分泌物并且提高在胰腺的损害表明激活的 oncogenic K 地岬。到 IL-6 或 histone H3 或为先进 glycation 的受体的大美人的抵销的抗体结束产品都限制表明激活的 K 地岬,阻止癌症开发和转移 / 侵略,并且延长在 Pdx1-Cre 的动物幸存; K 地岬 G12D/+;Hmgb1/ 鼠标。由 glycyrrhizin 的 HMGB1 损失的药理学抑制在煽动性的条件下面在老鼠限制 oncogenic K-Ras-driven tumorigenesis。减少在 PDAC 病人的 HMGB1 的原子、全部的细胞的表示与差的全面幸存相关,在 PDAC 与预示、治疗学的关联作为新奇肿瘤 suppressor 支持细胞内部的 HMGB1。 | Rui Kang Yangchun Xie Qiuhong Zhang Wen Hou Qingping Jiang Shan Zhu Jinbao Liu Dexing Zeng Haichao Wang David L Bartlet Timothy R Billiar Herbert J Zeh III Michael T Lotze Daolin Tang | 2017 | Cell Research2017，27，7： | 22 |
| 2 | Role of the IL-33-ST2 axis in sepsis显示文摘Sepsis remains a major clinical problem with high morbidity and mortality. As new inflammatory mediators are characterized, it is important to understand their roles in sepsis. Interleukin 33(IL-33) is a recently described member of the IL-1 family that is widely expressed in cells of barrier tissues. Upon tissue damage, IL-33 is released as an alarmin and activates various types of cells of both the innate and adaptive immune system through binding to the ST2/IL-1 receptor accessory protein complex. IL-33 has apparent pleiotropic functions in many disease models, with its actions strongly shaped by the local microenvironment. Recent studies have established a role for the IL-33-ST2 axis in the initiation and perpetuation of inflammation during endotoxemia, but its roles in sepsis appear to be organism and model dependent. In this review, we focus on the recent advances in understanding the role of the IL-33/ST2 axis in sepsis. | Hui Xu Heth R. Turnquist Rosemary Hoffman Timothy R. Billiar | 2017 | Military Medical Research2017，4，1： | 14 |
| 3 | High-mobility group box 1 protein is involved in the protective effect of Saquinavir on ventilation-induced lung injury in mice显示文摘 | Xin Wang Renlingzi Zhang Yao Tong Xibing Ding Shuqing Jin Xiang Zhao Jiaying Zong Zhixia Chen Timothy R. Billiar Quan Li | 2017 | Acta Biochimica et Biophysica Sinica2017，49，10： | 5 |
| 4 | Lung epithelial cell-derived IL-25 negatively regulates LPS-induced exosome release from macrophages显示文摘Background: Acute lung injury(ALI) is a major component of multiple organ dysfunction syndrome(MODS) following pulmonary and systemic infection. Alveolar macrophages(AMφ) are at the center of ALI pathogenesis. Emerging evidence has shown that cell-cell interactions in the lungs play an important regulatory role in the development of acute lung inflammation. However, the underneath mechanisms remain poorly addressed. In this study, we explore a novel function of lung epithelial cells(LEPCs) in regulating the release of exosomes from AMφ following LPS stimulation.Methods: For the in vivo experiments, C57 BL/6 wildtype(WT) mice were treated with lipopolysaccharide(LPS)(2 mg/kg) in 0.2 ml of saline via intratracheal aerosol administration. Bronchoalveolar lavage fluid was collected at 0–24 h after LPS treatment, and exosomes derived from AMφ were measured. For the in vitro studies, LEPCs and bone marrowderived Mφ(BMDM) were isolated from WT or TLR4-/-mice and were then cocultured in the Transwell? system. After coculture for 0–24 h, the BMDM and supernatant were harvested for the measurement of exosomes and cytokines.Results: We demonstrate that LPS induces macrophages(Mφ) to release exosomes, which are then internalized by neighboring Mφ to promote TNF-α expression. The secreted interleukin(IL)-25 from LEPCs downregulates Rab27 a and Rab27 b expression in Mφ, resulting in suppressed exosome release and thereby attenuating exosome-induced TNF-α expression and secretion.Conclusion: These findings reveal a previously unidentified crosstalk pathway between LEPCs and Mφ that negatively regulates the inflammatory responses of Mφ to LPS. Modulating IL-25 signaling and targeting exosome release may present a new therapeutic strategy for the treatment of ALI. | Zhi-Gang Li Melanie J. Scott Tomasz Brzóska Prithu Sundd Yue-Hua Li Timothy R. Billiar Mark A. Wilson Ping Wang Jie Fan | 2018 | Military Medical Research2018，5，4： | 5 |
| 5 | HMGB1 in health and disease显示文摘 | Rui Kang Ruochan Chen Qiuhong Zhang Wen Hou Sha Wu Lizhi Cao Jin Huang Yan Yu Xue-gong Fan Zhengwen Yan Xiaofang Sun Haichao Wang Qingde Wang Allan Tsung Timothy R. Billiar Herbert J. Zeh Michael T. Lotze Daolin Tang | 2014 | Molecular Aspects of Medicine2014，，： | 2 |
| 6 | Intracellular Hmgb1 Inhibits Inflammatory Nucleosome Release and Limits Acute Pancreatitis in Mice显示文摘 | Rui Kang Qiuhong Zhang Wen Hou Zhenwen Yan Ruochan Chen Jillian Bonaroti Preeti Bansal Timothy R. Billiar Allan Tsung Qingde Wang David L. Bartlett David C. Whitcomb Eugene B. Chang Xiaorong Zhu Haichao Wang Ben Lu Kevin J. Tracey Lizhi Cao Xue-Gong Fan M | 2013 | Gastroenterology2013，，： | 2 |
| 7 | Cysteine 230 Modulates Tumor Necrosis Factor-related Apoptosis-inducing Ligand Activity显示文摘 | BILLIAR TR | 2000 | Cancer Res2000，60，12： | 1 |
| 8 | Nitric oxide synthase gene transfer to the vessel wall显示文摘 | Kibbe M Billiar T Tzeng E | 1999 | Curr Opin Neohrol Hypertens1999，8，： | 1 |
| 9 | IFN-gamma inhibition of TRAIL-induced IAP-2 upregulation, a possible mechanism of IFN-gammaenhanced TRAIL-induced apoptosis 显示文摘 | Park SY Billiar TR Seol DW | 2002 | Biochem Biophys Res Commun2002，291，2： | 1 |
| 10 | Nitric oxide protects cultured rat hepatocytes from tumor necrosis factor-α reduced apoptosis by inducing heat shock protein 70 expression 显示文摘 | 9,Kim YM Watkins SC Billiar TR | 1997 | J Biol Chem1997，272，2： | 1 |
| 11 | Therapeutic Antioxidant Medical Gas显示文摘 | Nakao A Sugimoto R Billiar TR | 2009 | J Clin Biochem Nutr2009，44，1： | 1 |
| 12 | Activation of STAT proteins in the lung of rats following resuscitation from hem orrhagic shock显示文摘 | Hierholzer C Kalff JC Billiar TR | 1998 | Arch Orthop Trauma Surg1998，117，67： | 1 |
| 13 | Role of heme oxygenase 1 in TNF/TNF receptor-mediated apoptosis after hepatic ischemia/reper- fusion in rats 显示文摘 | Kim SJ Eum HA Billiar TR | 2013 | Shock2013，39，4： | 1 |
| 14 | Linking oxidative stress to inflammation:Toll-like receptors显示文摘 | Gil R Tsung A Billiar T | 2010 | Free Radic Biol Med2010，，9： | 1 |
| 15 | Linking oxidative stress to in- flammation : Toll-like receptors 显示文摘 | Gill R Tsung A Billiar T | 2010 | Free Radic Biol Med2010，48，9： | 1 |
| 16 | Nitric oxide as a bifunctional regulator of apoptosis 显示文摘 | Kim YM BoOk CA Billiar TR | 1999 | Circ Res1999，84，3： | 1 |
| 17 | Effects of exogenous and endogenous nitric oxide on mitochondrial of rat hepatocytes显示文摘 | Stadler J Billiar TR Curran RD | 1991 | Am J Physiol1991，260，： | 1 |
| 18 | Bist ability in apoptosis:roles of bax,bcl-2,and mitochondrial permeability transition pores显示文摘 | Bagci EZ Vodovotz Y Billiar TR | 2006 | Biophys J2006，90，： | 1 |
| 19 | Inducible nitric oxide synthase: from cloning to therapeutic applications显示文摘 | Schwentker A Billiar TR | 2002 | World J Surg2002，26，： | 1 |
| 20 | The secretable form of trimeric TRAIL a potent inducer of apoptosis显示文摘 | Kim MH Billiar TR Seol DW | 2004 | Biochemical and Biophysical Research Communications2004，321，4： | 1 |
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