Search results for: sTNF RI, human recombinant
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Autologous solution protects bovine cartilage explants from IL-1α- and TNFα-induced cartilage degradation.Osteoarthritis (OA) is characterized by deterioration of articular cartilage driven by an imbalance of pro- and anti-inflammatory cytokines. To address the cartilage deterioration observed in OA, an autologous protein solution (APS) has been developed which has been shown to inhibit the production of destructive proteases and inflammatory cytokines from chondrocytes and monocytes, respectively. The purpose of this study was to determine the chondroprotective effect of APS on IL-1α- or TNFα-challenged bovine articular cartilage explants. Cartilage explants were cultured in the presence or absence of recombinant inflammatory cytokines, IL-1α and TNFα. Explants under equivalent inflammatory conditions were pretreated with recombinant antagonists IL-1ra, sTNF-RI, or APS to measure their inhibition of matrix degradation. Explants were further evaluated with Safranin-O, Masson's Trichrome, and Hematoxylin and Eosin histological staining. APS was more effective than recombinant antagonists in preventing cartilage matrix degradation and inhibited any measurable IL-1α-induced collagen release over a 21-day culture period. APS treatment reduced the degree of Safranin-O staining loss when cartilage explants were cultured with IL-1α or TNFα. Micrographs of APS treated cartilage explants showed an increase in observed cellularity and apparent cell division. APS may have the potential to prevent cartilage loss associated with early OA.
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Blood-derived anti-inflammatory protein solution blocks the effect of IL-1β on human macrophages in vitro.The purpose of this research was to determine if an autologous protein solution (APS), prepared from platelet-rich plasma (PRP), could reduce the deleterious effects of inflammatory cytokines in vitro.
2998 related Products with: Blood-derived anti-inflammatory protein solution blocks the effect of IL-1β on human macrophages in vitro.Rabbit Anti-APIP Apaf1 In Human Macrophage Inflamma Human Macrophage Inflamma Goat Anti-Human Ribosomal Goat Anti-Human, Mouse GC Rabbit Anti-TNIP2 ABIN2 T Goat Anti-Human Vitamin D Proteins and Antibodies H Goat Anti-Human ribosomal Rabbit Anti-APIP Apaf1 In Human Macrophage Inflamma Rabbit Anti-Cell death in
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Evidence of a significant role for Fas-mediated apoptosis in HCV clearance during pegylated interferon plus ribavirin combination therapy.The role of apoptosis in treatment-induced HCV clearance is controversial. We sought to assess the kinetics of serum apoptosis-related cytokines during pegylated interferon-α2a or -α2b plus weight-based ribavirin therapy for genotype 1 chronic HCV infection.
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Autologous protein solution inhibits MMP-13 production by IL-1β and TNFα-stimulated human articular chondrocytes.Catabolic inflammatory cytokines are prevalent in osteoarthritis (OA). The purpose of this study was to evaluate an autologous protein solution (APS) as a potential chondroprotective agent for OA therapy. APS was prepared from platelet-rich plasma (PRP). The APS solution contained both anabolic (bFGF, TGF-β1, TGF-β2, EGF, IGF-1, PDGF-AB, PDGF-BB, and VEGF) and anti-inflammatory (IL-1ra, sTNF-RI, sTNF-RII, IL-4, IL-10, IL-13, and IFNγ) cytokines but low concentrations of catabolic cytokines (IL-1α, IL-1β, TNFα, IL-6, IL-8, IL-17, and IL-18). Human articular chondrocytes were pre-incubated with the antagonists IL-1ra, sTNF-RI, or APS prior to the addition of recombinant human IL-1β or TNFα. Following exposure to inflammatory cytokines, the levels of MMP-13 in the culture medium were evaluated by ELISA. MMP-13 production stimulated in chondrocytes by IL-1β or TNFα was reduced by rhIL-1ra and sTNF-RI to near basal levels. APS was also capable of inhibiting the production of MMP-13 induced by both IL-1β and TNFα. The combination of anabolic and anti-inflammatory cytokines in the APS created from PRP may render this formulation to be a potential candidate for the treatment of inflammation in patients at early stages of OA.
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TNF-alpha and shear stress-induced large artery adaptations.Tumor necrosis factor-alpha (TNF-alpha) up-regulation has been associated with both low and high shear-induced arterial remodeling. To address this apparent paradox and to define the biology of TNF-alpha signaling in large arteries, we tested the hypotheses that differential temporal expression of TNF-alpha drives shear-regulated arterial remodeling.
Epiandrosterone (3 beta H Recombinant Human SDF-1 a Rabbit Anti-CPLA2 alpha P alpha,alpha Diphenyl L pr PPAR-alpha Blocking Pepti Rabbit Anti-Proteasome 20 Rabbit anti Estrogen Rece Rabbit Anti-alpha-Synucle Mouse Anti-PKC alpha Anti Anti-AP-2 alpha Monoclona Jurkat Cell Extract (Indu Rabbit Anti-Insulin Recep
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Tumor necrosis factor-alpha and the early vein graft.Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-alpha activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-alpha therapy would inhibit NIH.
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Involvement of the TNF-alpha autocrine-paracrine loop, via NF-kappaB and YY1, in the regulation of tumor cell resistance to Fas-induced apoptosis.Many tumors are resistant to Fas ligand (FasL)-induced apoptosis. This study examined the role of tumor-derived TNF-alpha, via an autocrine/paracrine loop, in the regulation of tumor-cell resistance to FasL-induced apoptosis. We have reported that Fas expression and sensitivity to FasL is negatively regulated by the transcription repressor factor Yin Yang 1 (YY1). Thus, we hypothesized that tumor-derived TNF-alpha induces the activation of NF-kappaB and the transcription repressor YY1, both of which negatively regulate Fas expression and sensitivity to FasL-induced apoptosis. This hypothesis was tested in PC-3 prostate cancer cells which synthesize and secrete TNF-alpha and express constitutively active NF-kappaB and YY1. Treatment of PC-3 cells with TNF-alpha (10 units) resulted in increased NF-kappaB and YY1 DNA-binding activity, upregulation of YY1 expression, downregulation of surface and total Fas expression and enhanced resistance of PC-3 to apoptosis induced by the FasL agonist antibody CH-11. In contrast, blocking the binding of secreted TNF-alpha on PC-3 cells with soluble recombinant sTNF-RI resulted in significant inhibition of constitutive NF-kappaB and YY1 DNA-binding activity, downregulation of YY1 expression, upregulation of Fas expression and sensitization of tumor cells to CH-11-induced apoptosis. The regulation of YY1 expression and activity by NF-kappaB was demonstrated by the use of the NF-kappaB inhibitor Bay 11-7085 and by the use of a GFP reporter system whereby deletion of the YY1-tandem binding site in the promoter significantly enhanced GFP expression. The direct role of YY1 expression in the regulation of PC-3 resistance to CH-11-induced apoptosis was shown in cells transfected with siRNA YY1 whereby such cells exhibited upregulation of Fas expression and were sensitized to CH-11-induced apoptosis. These findings demonstrate that the TNF-alpha autocrine-paracrine loop is involved in the constitutive activation of the transcription factors NF-kappaB and YY1 in the tumor cells and this loop leads to inhibition of Fas expression and resistance to FasL-induced apoptosis. Further, these findings identify new targets such as TNF-alpha, NF-kappaB and YY1, whose inhibition can reverse tumor cell resistance to FasL-mediated apoptosis.
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Protein-solute interactions affect the outcome of ultrafiltration/diafiltration operations.Protein production operations often involve a final diafiltration of the protein into formulation buffer. For several Amgen product proteins, post-diafiltration assays revealed a significant difference in molar excipient concentrations on the retentate and the permeate side of the membrane. For example, post-diafiltration assays of formulated 200 mg/mL human interleukin-1 receptor antagonist showed molar chloride concentrations up to 30% lower than those of the diafiltration buffer. Deviations from expected results were also observed in cases where a fusion conjugate protein (AMG-719) was formulated by dialysis in 10 mM acetate and where PEGylated soluble tumor necrosis factor receptor (PEG-sTNF-RI) was formulated in 270 mM glycine and 10 mM histidine. Classical thermodynamic theory describing intermolecular interactions predicts that the partitioning of small solutes during dialysis will be dependent on the protein concentration, charge, and surface area. This study illustrates methods to approximate these effects using readily available protein data (theoretical titration curves based on protein sequence, density information, etc.). Additionally, guidelines are provided to determine when intermolecular interactions are likely to significantly impact the outcome of dialysis/diafiltration operations.
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Design of PEGylated soluble tumor necrosis factor receptor type I (PEG sTNF-RI) for chronic inflammatory diseases.A recombinant C-terminal truncated form of the human soluble tumor necrosis factor receptor type I (sTNF-RI) was produced in E. coli. This soluble receptor contains the first 2.6 of the 4 domains of the intact sTNF-RI molecule. A monoPEGylated form of this molecule was produced using a 30 kD methoxyPEG aldehyde with approximately 85% selectivity for the N-terminal amino group. This molecule was shown to be less immunogenic in primates than the full length (4.0 domain) molecule or other versions of sTNF-RI which were either PEGylated at different sites or with different molecular weight PEGs. The 30 kD PEG also has a longer serum half-life to the molecule than lower molecular weight PEGs. This molecule markedly blunts the inflammatory response in a number of rheumatoid arthritis animal models. In addition, phase I/II and early phase II data in humans indicate that PEG sTNF-RI is non-immunogenic and that weekly dosing with this drug can reduce the number of tender and swollen joints in rheumatoid arthritis patients. PEG sTNF-RI has comparable American College of Rheumatology (ACR) efficacy scores as other anti-TNF molecules currently used to treat rheumatoid arthritic patients.
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Effects of a PEGylated soluble TNF receptor type 1 (PEG sTNF-RI) on cytokine expression in adjuvant arthritis.To investigate the effects of TNF blocking therapy on synovial immune activity in rat adjuvant arthritis (AA) by measuring mRNA expression of key macrophage and T cell cytokines during PEG sTNF-RI treatment (10mg/kg) on days 8, 10 and 12.
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