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      1. Author :
        Evans, L.; Williams, A.S.; Hayes, A.J.; Jones, S.A.; Nowell, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Arthritis and Rheumatism
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apo866; Arthritis; In vivo; Living Image software; MMPSense 750 FAST; Xenogen Caliper IVIS 200
      12. Abstract :
        OBJECTIVE: Using APO866, studies assessed the ability of Pre-B-cell colony-Enhancing Factor (PBEF) to regulate inflammatory and degradative processes in fibroblasts and collagen-induced arthritis. METHODS: ELISAs were used to examine regulation of metalloproteinases and chemokine expression by HFF fibroblasts. PBEF was further examined in the collagen-induced arthritis model using APO866. Disease activity was assessed using radiography, histology, in vivo imaging and quantitative PCR (qPCR). RESULTS: In vitro activation of fibroblasts with PBEF promoted MMP-3, CCL-2 and CXCL-8 expression, an effect inhibited by APO866. Early intervention with APO866 in collagen-induced arthritis inhibited both synovial inflammation, including chemokine-directed leukocyte infiltration, and the systemic marker of inflammation, serum hyaluronic acid. Blockade of degenerative processes by APO866 was further illustrated by the reduced expression of MMP-3 and MMP-13 in joint extracts and reduction of the systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein (COMP). Radiology showed that APO866 protected against bone erosion, whilst qPCR demonstrated inhibition of RANKL expression. APO866 treatment in established disease (clinical score >=5) reduced synovial inflammation, cartilage destruction and halted bone erosion. MMP-3, CCL-2 and RANKL activity, as assessed by in vivo imaging with MMPSense750 and qPCR were reduced in treated animals. qPCR of synovial explants from animals with CIA showed that APO866 inhibited MMP-3, CCL-2 and RANKL production, a result that was reversed with nicotinamide mononucleotide (NMN) CONCLUSIONS: These data confirm PBEF to be an important regulator of inflammation, cartilage catabolism and bone erosion, and highlights APO866 as a promising therapy for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ user @ 8551
      15. Serial :
        4800
      1. Author :
        Laurie E. Littlepage; Mark D. Sternlicht; Nathalie Rougier; Joanna Phillips; Eugenio Gallo; Ying Yu; Kurt Williams; Audrey Brenot; Jeffrey I. Gordon; Zena Werb
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer Research
      6. Products :
      7. Volume :
        70
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        matrix metalloproteinase; neuroendocrine; prostate cancer; metatasis
      12. Abstract :
        Prostate cancer is the leading form of cancer in men. Prostate tumors often contain neuroendocrine differentiation, which correlates with androgen-independent progression and poor prognosis. Matrix metalloproteinases (MMP), a family of enzymes that remodel the microenvironment, are associated with tumorigenesis and metastasis. To evaluate MMPs during metastatic prostatic neuroendocrine cancer development, we used transgenic mice expressing SV40 large T antigen in their prostatic neuroendocrine cells, under the control of transcriptional regulatory elements from the mouse cryptdin-2 gene (CR2-TAg). These mice have a stereotypical pattern of tumorigenesis and metastasis. MMP-2, MMP-7, and MMP-9 activities increased concurrently with the transition to invasive metastatic carcinoma, but they were expressed in different prostatic cell types: stromal, luminal epithelium, and macrophages, respectively. CR2-TAg mice treated with AG3340/Prinomastat, an MMP inhibitor that blocks activity of MMP-2, MMP-9, MMP-13, and MMP-14, had reduced tumor burden. CR2-TAg animals were crossed to mice homozygous for null alleles of MMP-2, MMP-7, or MMP-9 genes. At 24 weeks CR2-TAg; MMP-2-/- mice showed reduced tumor burden, prolonged survival, decreased lung metastasis, and decreased blood vessel density, whereas deficiencies in MMP-7 or MMP-9 did not influence tumor growth or survival. Mice deficient for MMP-7 had reduced endothelial area coverage and decreased vessel size, and mice lacking MMP-9 had increased numbers of invasive foci and increased perivascular invasion, as well as decreased tumor blood vessel size. Together, these results suggest distinct contributions by MMPs to the progression of aggressive prostate tumor and to helping tumors cleverly find alternative routes to malignant progression.
      13. URL :
        http://cancerres.aacrjournals.org/content/70/6/2224.abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4490
      1. Author :
        Clapper, M. L.; Hensley, H. H.; Chang, W. C.; Devarajan, K.; Nguyen, M. T.; Cooper, H. S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Neoplasia
      6. Products :
      7. Volume :
        13
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Adenoma/diagnosis/*enzymology/pathology; Animals; Colorectal Neoplasms/diagnosis/*enzymology/pathology; Disease Models, Animal; Female; *Fluorescent Dyes/administration & dosage/diagnostic use; Male; Matrix Metalloproteinases/*metabolism; Mice; Mice, Inbred C57BL; Molecular Imaging
      12. Abstract :
        A significant proportion of colorectal adenomas, in particular those that lack an elevated growth component, continue to escape detection during endoscopic surveillance. Elevation of the activity of matrix metalloproteinases (MMPs), a large family of zinc endopeptidases, in adenomas serves as a biomarker of early tumorigenesis. The goal of this study was to assess the feasibility of using a newly developed near-infrared bioactivatable probe (MMPSense 680) that reports the activity of a broad array of MMP isoforms to detect early colorectal adenomas. Adenomatous polyposis coli (Apc)(+/Min-FCCC) mice that spontaneously develop multiple colorectal adenomas were injected with MMPSense 680, and the colons were imaged in an IVIS Spectrum system ex vivo. Image analyses were correlated with histopathologic findings for all regions of interest (ROIs). The biochemical basis of fluorescent signal was investigated by immunohistochemical staining of MMP-7 and -9. A strong correlation (Kendall = 0.80) was observed between a positive signal and the presence of pathologically confirmed colonic adenomas; 92.9% of the 350 ROIs evaluated were classified correctly. The correlation between two independent observers was 0.87. MMP-7 expression was localized to epithelial cells of adenomas and microadenomas, whereas staining of MMP-9 was found in infiltrating polymorphonuclear leukocytes within the adenomas. MMPSense 680 identifies colorectal adenomas, both polypoid and nonpolypoid, in Apc(+/Min-FCCC) mice with high specificity. Use of this fluorescent probe in combination with colonoscopy could aid in preventing colorectal neoplasias by providing new opportunities for early detection and therapeutic intervention.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21847360
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10459
      1. Author :
        Evans, L.; Williams, A. S.; Hayes, A. J.; Jones, S. A.; Nowell, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Arthritis Rheum
      6. Products :
      7. Volume :
        63
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Acrylamides/pharmacology/*therapeutic use; Animals; Arthritis, Experimental/*drug therapy/metabolism/pathology; Cartilage/*metabolism/pathology; Fibroblasts/metabolism/pathology; Humans; Inflammation/metabolism/pathology; Leukocytes/*drug effects/metabolism/pathology; Mice; Nicotinamide Phosphoribosyltransferase/*antagonists & inhibitors; Piperidines/pharmacology/*therapeutic use
      12. Abstract :
        OBJECTIVE: To assess the ability of pre-B cell colony-enhancing factor (PBEF) to regulate inflammation and degradative processes in inflammatory arthritis, using the small molecule inhibitor APO866 in human fibroblasts in vitro and in murine collagen-induced arthritis (CIA). METHODS: Enzyme-linked immunosorbent assays were used to examine regulation of expression of metalloproteinases and chemokines in human fibroblasts. The role of PBEF was further examined using APO866 in mice with CIA, with effects on disease activity assessed using radiography, histology, in vivo imaging, and quantitative polymerase chain reaction (qPCR). RESULTS: In vitro activation of human fibroblasts with PBEF promoted expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an effect inhibited by APO866. In mice with CIA, early intervention with APO866 inhibited synovial inflammation, including chemokine-directed leukocyte infiltration, and reduced a systemic marker of inflammation, serum hyaluronic acid. APO866 blockade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in a systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein. Radiologic images revealed that APO866 protected against bone erosion, while qPCR demonstrated inhibition of RANKL expression. In mice with established disease, APO866 reduced synovial inflammation and cartilage destruction, and halted bone erosion. In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide. CONCLUSION: These findings confirm PBEF to be an important regulator of inflammation, cartilage catabolism, and bone erosion, and highlight APO866 as a promising therapeutic agent for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10460
      1. Author :
        Hsieh, C. H.; Chang, H. T.; Shen, W. C.; Shyu, W. C.; Liu, R. S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Mol Imaging Biol
      6. Products :
      7. Volume :
        14
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Animals; Cell Hypoxia; Cell Line, Tumor; Cell Movement; Enzyme Activation; Extracellular Signal-Regulated MAP Kinases/metabolism; Gene Knockdown Techniques; Glioblastoma/*enzymology/*pathology; Humans; JNK Mitogen-Activated Protein Kinases/metabolism; Matrix Metalloproteinase 9/metabolism; Mice; Mice, SCID; Molecular Imaging/*methods; NADPH Oxidase/*metabolism; NF-kappa B/metabolism; Neoplasm Invasiveness; Reactive Oxygen Species/metabolism; Tumor Microenvironment; Xenograft Model Antitumor Assays
      12. Abstract :
        PURPOSE: We determined the impact of the cycling hypoxia tumor microenvironment on tumor cell invasion and infiltration in U87 human glioblastoma cells and investigated the underlying mechanisms using molecular bio-techniques and imaging. PROCEDURES: The invasive phenotype of U87 cells and xenografts exposed to experimentally imposed cycling hypoxic stress in vitro and in vivo was determined by the matrigel invasion assay in vitro and dual optical reporter gene imaging in vivo. RNAi-knockdown technology was utilized to study the role of the NADPH oxidase subunit 4 (Nox4) on cycling hypoxia-mediated tumor invasion. RESULTS: Cycling hypoxic stress significantly promoted tumor invasion in vitro and in vivo. However, Nox4 knockdown inhibited this effect. Nox4-generated reactive oxygen species (ROS) are required for cycling hypoxia-induced invasive potential in U87 cells through the activation of NF-kappaB- and ERK-mediated stimulation of MMP-9. CONCLUSIONS: Cycling hypoxia-induced ROS via Nox4 should be considered for therapeutic targeting of tumor cell invasion and infiltration in glioblastoma.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21870211
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10461
      1. Author :
        Ibarra, J. M.; Jimenez, F.; Martinez, H. G.; Clark, K.; Ahuja, S. S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Int J Inflam
      6. Products :
      7. Volume :
        2011
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS
      12. Abstract :
        The Standard measures of experimental arthritis fail to detect, visualize, and quantify early inflammation and disease activity. Here, we describe the use of an injectable MMP-activated fluorescence agent for in vivo quantification of acute inflammation produced by collagen-antibody-induced arthritis (CAIA) in CC chemokine receptor-2 (Ccr2(-/-)) null mice. Although Ccr2(-/-) DBA1/J mice were highly susceptible to and rapidly developed CAIA, the standard clinical assessment of fore or hind paw thicknesses was unable to detect significant acute inflammatory changes (days 3-10). Remarkably, noninvasive, in situ, MMP-activatable fluorescent imaging of Ccr2(-/-) DBA1/J mice with CAIA displayed acute joint pathology in advance of clinically measurable acute inflammation (days 5, 7, and 10). These results were confirmed by the histology of ankle joints, which showed significant inflammation, bone loss, and synovial hyperplasia, compared to control mice at postimmunization day 5. The MMP-mediated fluorescence technique holds tremendous implications for quantifiable examination of arthritis disease activity of acute joint inflammation.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21755029
      14. Call Number :
        PKI @ kd.modi @ 4
      15. Serial :
        10462
      1. Author :
        Wallis de Vries, B. M.; van Dam, G. M.; Tio, R. A.; Hillebrands, J. L.; Slart, R. H.; Zeebregts, C. J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        J Vasc Surg
      6. Products :
      7. Volume :
        48
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Atherosclerosis/complications/*diagnosis; Carotid Stenosis/*diagnosis/etiology; Diagnostic Imaging/*methods; Humans; Reproducibility of Results
      12. Abstract :
        BACKGROUND: There is increasing evidence that plaque vulnerability, rather than the degree of stenosis, is important in predicting the occurrence of subsequent cerebral ischemic events in patients with carotid artery stenosis. The many imaging modalities currently available have different properties with regard to the visualization of the extent of vulnerability in carotid plaque formation. METHODS: Original published studies were identified using the MEDLINE database (January 1966 to March 2008). Manual cross-referencing was also performed. RESULTS: There is no single imaging modality that can produce definitive information about the state of vulnerability of an atherosclerotic plaque. Each has its own specific drawbacks, which may be the use of ionizing radiation or nephrotoxic contrast agents, an invasive character, low patient tolerability, or simply the paucity of information obtained on plaque vulnerability. Functional molecular imaging techniques such as positron emission tomography (PET), single photon emission-computed tomography (SPECT) and near infra-red spectroscopy (NIRS) do seem able accurately to visualize and even quantify features of plaque vulnerability and its pathophysiologic processes. Promising new techniques like near infra-red fluorescence imaging are being developed and may be beneficial in this field. CONCLUSION: There is a promising role for functional molecular imaging modalities like PET, SPECT, or NIRS related to improvement of selection criteria for carotid intervention, especially when combined with CT or MRI to add further anatomical details to molecular information. Further information will be needed to define whether and where this functional molecular imaging will fit into a clinical strategy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18804942
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10464
      1. Author :
        G. Blum
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Current Opinion in Drug Discovery Development
      6. Products :
      7. Volume :
        10
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Biology; Cancer
      11. Keywords :
        Proteases; pathology; biological markers; fluorescence imaging reagents; in vivo imaging; fluorescence molecular tomography; FMT
      12. Abstract :
        Proteases play pivotal roles in the normal function of cells. In addition, the expression and activity of proteases are significantly upregulated in several pathologies, including cancer, arthritis and atherosclerosis, and hence they can be considered to be biological markers for these pathologies. The hydrolyzing activity of proteases has been used to generate a variety of fluorescent imaging reagents, the design and utility of which are reviewed here. The use of imaging reagents to visualize protease activity allows for improved detection of various pathologies as well as the ability to monitor the efficacy of therapies in vivo and provide molecular information regarding the nature of the pathology.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18729022
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4475
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