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MOUSE ANTI HUMAN VON WILLEBRAND FACTOR

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[#ABS11989] MOUSE ANTI HUMAN VON WILLEBRAND FACTOR

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ABS11989 | MOUSE ANTI HUMAN VON WILLEBRAND FACTOR , 0.5 mg
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(1) Influence of Phosphatidylinositol-3-Kinase/Protein Kinase B-Mammalian Target of Rapamycin Signaling Pathway on the Neuropathic Pain Complicated by Nucleoside Reverse Transcriptase Inhibitors for the Treatment of HIV Infection.[TOP]

Pubmed ID :30058583
Publication Date : //
Nucleoside reverse transcriptase inhibitors (NRTIs) are the earliest and most commonly used anti-human immunodeficiency virus drugs and play an important role in high active antiretroviral therapy. However, NRTI drug therapy can cause peripheral neuropathic pain. In this study, we aimed to investigate the mechanisms of rapamycin on the pain sensitization of model mice by in vivo experiments to explore the effect of mammalian target of rapamycin (mTOR) in the pathogenesis of neuropathic pain caused by NRTIs.

Authors : Cheng Hao, Wu Liang-Yu,



(2) Discovery of a benzenesulfonamide-based dual inhibitor of microsomal prostaglandin E synthase-1 and 5-lipoxygenase that favorably modulates lipid mediator biosynthesis in inflammation.[TOP]

Pubmed ID :30053720
Publication Date : //
Leukotrienes (LTs) and prostaglandin (PG)E, produced by 5-lipoxygenase (5-LO) and microsomal prostaglandin E synthase-1 (mPGES-1), respectively, are key players in inflammation, and pharmacological suppression of these lipid mediators (LM) represents a strategy to intervene with inflammatory disorders. Previous studies revealed that the benzenesulfonamide scaffold displays efficient 5-LO-inhibitory properties. Here, we structurally optimized benzenesulfonamides which led to an N-phenylbenzenesulfonamide derivative (compound 47) with potent inhibitory activities (IC = 2.3 and 0.4 μM for isolated 5-LO and 5-LO in intact cells, respectively). Compound 47 prevented the interaction of 5-LO with its activating protein (FLAP) at the nuclear envelope in transfected HEK293 cells as shown by in situ proximity ligation assay. Comprehensive assessment of the LM profile produced by human macrophages revealed the ability of 47 to selectively down-regulate pro-inflammatory LMs (i.e. LTs and PGE) in M1 but to enhance the formation of pro-resolving LMs (i.e. resolvins and maresins) in M2 macrophages. Moreover, 47 strongly inhibited LT formation and cell infiltration in two in vivo models of acute inflammation (i.e., peritonitis and air pouch sterile inflammation in mice). Together, 47 represents a novel LT biosynthesis inhibitor with an attractive pharmacological profile as anti-inflammatory drug that also promotes the biosynthesis of pro-resolving LM.

Authors : Cheung Sun-Yee, Werner Markus, Esposito Lucia, Troisi Fabiana, Cantone Vincenza, Liening Stefanie, König Stefanie, Gerstmeier Jana, Koeberle Andreas, Bilancia Rossella, Rizza Roberta, Rossi Antonietta, Roviezzo Fiorentina, Temml Veronika, Schuster Daniela, Stuppner Hermann, Schubert-Zsilavecz Manfred, Werz Oliver, Hanke Thomas, Pace Simona,



(3) The role of Sprouty1 in the proliferation, differentiation and apoptosis of epidermal keratinocytes.[TOP]

Pubmed ID :30039569
Publication Date : //
Sprouty (SPRY) 1 is one of the SPRY proteins that inhibits signalling from various growth factors pathways and has also been known as a tumour suppressor in various malignancies. However, no study elucidates the role of SPRY1 in the skin. Our study was conducted to determine the function of SPRY1 in human keratinocytes and the epidermis.

Authors : Wang Ping, Zhou Yuan, Yang Jian-Qiang, Landeck Lilla, Min Min, Chen Xi-Bei, Chen Jia-Qi, Li Wei, Cai Sui-Qing, Zheng Min, Man Xiao-Yong,



(4) No Significant Role for Smooth Muscle Cell Mineralocorticoid Receptors in Atherosclerosis in the Apolipoprotein-E Knockout Mouse Model.[TOP]

Pubmed ID :30038907
Publication Date : //
Elevated levels of the hormone aldosterone are associated with increased risk of myocardial infarction and stroke in humans and increased progression and inflammation of atherosclerotic plaques in animal models. Aldosterone acts through the mineralocorticoid receptor (MR) which is expressed in vascular smooth muscle cells (SMCs) where it promotes SMC calcification and chemokine secretion . The objective of this study is to explore the role of the MR specifically in SMCs in the progression of atherosclerosis and the associated vascular inflammation in the apolipoprotein E knockout (ApoE) mouse model. Male ApoE mice were bred with mice in which MR could be deleted specifically from SMCs by tamoxifen injection. The resulting atheroprone SMC-MR-KO mice were compared to their MR-Intact littermates after high fat diet (HFD) feeding for 8 or 16 weeks or normal diet for 12 months. Body weight, tail cuff blood pressure, heart and spleen weight, and serum levels of glucose, cholesterol, and aldosterone were measured for all mice at the end of the treatment period. Serial histologic sections of the aortic root were stained with Oil Red O to assess plaque size, lipid content, and necrotic core area; with PicroSirius Red for quantification of collagen content; by immunofluorescent staining with anti-Mac2/Galectin-3 and anti-smooth muscle α-actin antibodies to assess inflammation and SMC marker expression; and with Von Kossa stain to detect plaque calcification. In the 16-week HFD study, these analyses were also performed in sections from the brachiocephalic artery. Flow cytometry of cell suspensions derived from the aortic arch was also performed to quantify vascular inflammation after 8 and 16 weeks of HFD. Deletion of the MR specifically from SMCs did not significantly change plaque size, lipid content, necrotic core, collagen content, inflammatory staining, actin staining, or calcification, nor were there differences in the extent of vascular inflammation between MR-Intact and SMC-MR-KO mice in the three experiments. SMC-MR does not directly contribute to the formation, progression, or inflammation of atherosclerotic plaques in the ApoE mouse model of atherosclerosis. This indicates that the MR in non-SMCs mediates the pro-atherogenic effects of MR activation.

Authors : Moss M Elizabeth, DuPont Jennifer J, Iyer Surabhi L, McGraw Adam P, Jaffe Iris Z,



(5) Anti-inflammatory Effects of the Octapeptide NAP in Human Microbiota-Associated Mice Suffering from Subacute Ileitis.[TOP]

Pubmed ID :29997909
Publication Date : //
The octapeptide NAP is well known for its neuroprotective properties. We here investigated whether NAP treatment could alleviate pro-inflammatory immune responses during experimental subacute ileitis. To address this, mice with a human gut microbiota were perorally infected with one cyst of (day 0) and subjected to intraperitoneal synthetic NAP treatment from day 1 until day 8 postinfection (p.i.). Whereas placebo (PLC) control animals displayed subacute ileitis at day 9 p.i., NAP-treated mice exhibited less pronounced pro-inflammatory immune responses as indicated by lower numbers of intestinal mucosal T and B lymphocytes and lower interferon (IFN)- concentrations in mesenteric lymph nodes. The NAP-induced anti-inflammatory effects were not restricted to the intestinal tract but could also be observed in extra-intestinal including systemic compartments, given that pro-inflammatory cytokines were lower in liver, kidney, and lung following NAP as compared to PLC application, whereas at day 9 p.i., colonic and serum interleukin (IL)-10 concentrations were higher in the former as compared to the latter. Remarkably, probiotic commensal bifidobacterial loads were higher in the ileal lumen of NAP as compared to PLC-treated mice with ileitis. Our findings thus further support that NAP might be regarded as future treatment option directed against intestinal inflammation.

Authors : Escher Ulrike, Giladi Eliezer, Dunay Ildikò R, Bereswill Stefan, Gozes Illana, Heimesaat Markus M,



(6) CEACAM1 promotes CD8 T cell responses and improves control of a chronic viral infection.[TOP]

Pubmed ID :29967450
Publication Date : //
Dysfunction of CD8 T cells can lead to the development of chronic viral infection. Identifying mechanisms responsible for such T cell dysfunction is therefore of great importance to understand how to prevent persistent viral infection. Here we show using lymphocytic choriomeningitis virus (LCMV) infection that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is fundamental for recruiting lymphocyte-specific protein kinase (Lck) into the T cell receptor complex to form an efficient immunological synapse. CEACAM1 is essential for activation of CD8 T cells, and the absence of CEACAM1 on virus-specific CD8 T cells limits the antiviral CD8 T cell response. Treatment with anti-CEACAM1 antibody stabilizes Lck in the immunological synapse, prevents CD8 T cell exhaustion, and improves control of virus infection in vivo. Treatment of human virus-specific CD8 T cells with anti-CEACAM1 antibody similarly enhances their proliferation. We conclude that CEACAM1 is an important regulator of virus-specific CD8 T cell functions in mice and humans and represents a promising therapeutic target for modulating CD8 T cells.

Authors : Khairnar Vishal, Duhan Vikas, Patil Ashwini M, Zhou Fan, Bhat Hilal, Thoens Christine, Sharma Piyush, Adomati Tom, Friendrich Sarah-Kim, Bezgovsek Judith, Dreesen Janine D, Wennemuth Gunther, Westendorf Astrid M, Zelinskyy Gennadiy, Dittmer Ulf, Hardt Cornelia, Timm Jörg, Göthert Joachim R, Lang Philipp A, Singer Bernhard B, Lang Karl S,



(7) Anti-inflammatory nitro-fatty acids suppress tumor growth by triggering mitochondrial dysfunction and activation of the intrinsic apoptotic pathway in colorectal cancer cells.[TOP]

Pubmed ID :29909078
Publication Date : //
Nitro-fatty acids (NFAs) are endogenously occurring lipid mediators exerting strong anti-inflammatory effects and acting as anti-oxidants in a number of animal models of inflammation. These NFA effects are mediated by targeting important regulatory proteins involved in inflammatory processes, such as 5-lipoxygenase, soluble epoxide hydrolase, or NF-κB. In the present study, we investigated the anti-tumorigenic effects of NFAs on colorectal cancer (CRC) cells in cell culture-based experiments and in a murine xenograft model of human CRC. We could show that 9-NOA suppresses the viability of CRC cells (HCT-116 and HT-29) by inducing a caspase-dependent apoptosis via the intrinsic apoptotic pathway. Co-treatment with the pan-caspase inhibitor Q-VD-OPH counteracted the NFA-mediated apoptosis in both cell lines. Furthermore, NFAs affected the cell cycle transition and reduced the oxygen consumption rate (OCR) immediately. On the contrary to their well-known anti-oxidative properties, NFAs mediated the generation of mitochondrial oxidative stress in human CRC cells. Additionally, similar to the cytostatic drug mitomycin, 9-NOA significantly reduced tumor growth in a murine xenograft model of human colorectal cancer. In contrast to the established cytostatic drug, 9-NOA treatment was well tolerated by mice. This study delivers a novel mechanistic approach for nitro-fatty acid-induced inhibition of CRC cell growth by targeting mitochondrial functions such as the mitochondrial membrane potential and mitochondrial respiration. We suggest these naturally occurring lipid mediators as a new class of well tolerated chemotherapeutic drug candidates for treatment of CRC or potentially other inflammation-driven cancer types.

Authors : Kühn Benjamin, Brat Camilla, Fettel Jasmin, Hellmuth Nadine, Maucher Isabelle V, Bulut Ufuk, Hock Katharina J, Grimmer Jennifer, Manolikakes Georg, Rühl Michael, Kühn Alessa, Zacharowski Kai, Matrone Carmela, Urbschat Anja, Roos Jessica, Steinhilber Dieter, Maier Thorsten J,



(8) Ganoderma Triterpenoids Exert Antiatherogenic Effects in Mice by Alleviating Disturbed Flow-Induced Oxidative Stress and Inflammation.[TOP]

Pubmed ID :29849882
Publication Date : //
Ganoderma mushrooms, used in traditional Chinese medicine to promote health and longevity, have become widely accepted as herbal supplements. (GL), a commonly seen ganoderma species, is commercially cultivated under controlled conditions for more consistent chemical composition. The medicinal properties of GL are attributable to its antioxidant and anti-inflammatory activities. We intended to assess the effect of GL in atherosclerosis, an arterial condition associated with chronic oxidative stress and inflammation, using a carotid-artery-ligation mouse model. Flow turbulence created in the ligated artery induces oxidative stress and neointimal hyperplasia, a feature of early atherogenesis. Daily oral GL prevented neointimal thickening 2 weeks after ligation. Moreover, the ganoderma triterpenoid (GT) crude extract isolated from GL abolished ligation-induced neointima formation. Mechanistically, endothelial dysfunction was observed 3 days after ligation before any structural changes could be detected. GTs alleviated the oxidative stress and restored the atheroresistent status of endothelium by inhibiting the induction of a series of atherogenic factors, including endothelin-1, von Willebrand factor, and monocyte chemoattractant protein-1 after 3-day ligation. The anti-inflammatory activity of GTs was tested in cultured human umbilical vein endothelial cells (HUVECs) exposed to disturbed flow in an perfusion system. GTs abolished the induction of proinflammatory VCAM-1, TNF-, and IL-6 by oscillatory shear stress. Moreover, the antioxidant activity of GTs was tested in HUVECs against the insult of HO. GTs dissipated the cellular superoxide accumulation imposed by HO, thereby mitigating HO-induced cell damage and proatherogenic response. Our results revealed the atheroprotective properties of ganoderma mushrooms and identified triterpenoids as the critical constituents for those effects. GTs prevent atherogenesis by eliminating disturbed flow-induced oxidative stress and inflammation.

Authors : Hsu Pei-Ling, Lin Yung-Ching, Ni Hao, Mo Fan-E,



(9) Knockout of microRNA-21 attenuates alcoholic hepatitis through VHL/NF-κB signaling pathway in hepatic stellate cells.[TOP]

Pubmed ID :29848019
Publication Date : //
microRNA-21 is one of the most abundant miRNAs in chronic liver injuries including alcoholic liver injury. Previous studies have demonstrated that miR-21 plays a role in inflammation in the liver and functions in hepatic stellate cells (HSCs), which reside in the perisinusoidal space between sinusoidal endothelial cells and hepatocytes and regulate sinusoidal circulation. HSCs integrate cytokine-mediated inflammatory responses in the sinusoids and relay them to the liver parenchyma. Here, we showed that the activation of Von Hippel-Lindau (VHL) expression, by miR-21 knockout in vivo and anti-miR-21 or VHL overexpression in vitro, suppressed the production of proinflammatory cytokines, such as interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1) and IL-1β, in human hepatic stellate cells during alcoholic liver injury. Sequence and functional analyses confirmed that miR-21 directly targeted the 3'-untranslated region of VHL. Immunofluorescence and real-time PCR analysis revealed that miR-21 depletion blocked NF-κB activation in human HSCs both in cultured HSCs as well as HSCs isolated from ALD mice liver by laser capture microdissection. We also showed that conditioned medium from anti-miR-21-transfected HSCs suppressed human monocyte-derived THP-1 cell migration. Taken together, our study indicates that depletion of miR-21 may downregulate cytokine production in HSCs and macrophage chemotaxis during alcoholic liver injury and that the targeting of miR-21 may have therapeutic potential for preventing the progression of alcoholic liver diseases.

Authors : Wu Nan, McDaniel Kelly, Zhou Tianhao, Ramos-Lorenzo Sugeily, Wu Chaodong, Huang Li, Chen Demeng, Annable Tami, Francis Heather, Glaser Shannon, Alpini Gianfranco, Meng Fanyin,



(10) Humanization of bone and bone marrow in an orthotopic site reveals new potential therapeutic targets in osteosarcoma.[TOP]

Pubmed ID :29705656
Publication Date : //
Existing preclinical murine models often fail to predict effects of anti-cancer drugs. In order to minimize interspecies-differences between murine hosts and human bone tumors of in vivo xenograft platforms, we tissue-engineered a novel orthotopic humanized bone model.

Authors : Wagner Ferdinand, Holzapfel Boris M, McGovern Jacqui A, Shafiee Abbas, Baldwin Jeremy G, Martine Laure C, Lahr Christoph A, Wunner Felix M, Friis Thor, Bas Onur, Boxberg Melanie, Prodinger Peter M, Shokoohmand Ali, Moi Davide, Mazzieri Roberta, Loessner Daniela, Hutmacher Dietmar W,