Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue-specific localization of HIV-1-infected lymphoid cells may contribute to clinical manifestations of AIDS. Therefore we investigated the effect of HIV-1 infection on mechanisms of T lymphocyte invasion, a process required for movement of cells into and out of the circulation. In the present study, we demonstrate that HIV-1-infected human lymphocytes secrete increased amounts of the human 92-kDa type IV collagenase when compared to uninfected lymphocytes. Furthermore, HIV-1-infected lymphocytes degrade the extracellular matrix proteins collagen IV and fibronectin, and they are more invasive through a reconstituted basement membrane when compared to uninfected cells. The addition of either antibody to the 92-kDa collagenase or TIMP-2, a type IV collagenase inhibitor, abolishes invasive activity. These data suggest that HIV-1-infected lymphocytes express phenotypic characteristics that are consistent with an enhanced ability to leave the circulation and to localize in target tissues. Local viral infection or the release of viral proteins, cytokines, or proteolytic enzymes in tissues may contribute to pathogenesis.
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PMID:HIV-1 infection stimulates T cell invasiveness and synthesis of the 92-kDa type IV collagenase. 834 96

We showed previously that human malignant non-Hodgkin's lymphomas (NHL) degrade extracellular matrix (ECM) components through the action of metalloproteinases and that elevated expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) correlated with a poor clinical outcome in patients with NHL. In the present study we sought to investigate whether there is any correlation between the expression of gelatinases (MMP-2 and MMP-9), TIMP-1, and the expression of cytokines and growth factors such as interleukin-1beta (IL-1beta), IL-6, IL-10, tumor necrosis factor alpha (TNF-alpha), transforming growth factor beta (TGFbeta), and basic fibroblast growth factor (bFGF) in human NHL. In lymphoma tissues obtained from 32 patients, elevated expression of IL-6 correlated significantly with elevated messenger RNA (mRNA) levels of MMP-9, MMP-2, and TIMP-1. Moreover, in human lymphoid cell lines of B- and T-cell origin (Raji, Jurkat, and NC-37), IL-6 stimulated production of MMP-9 and MMP-2 but not TIMP-1. In the Matrigel invasion assay IL-6 significantly upregulated transmigration of Raji and Jurkat cells, which in turn was inhibited by recombinant human TIMP-1 and anti-MMP-9 and MMP-2 antibodies. We postulate that IL-6 may play a role in the clinical aggressiveness of human NHL by stimulating MMP production.
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PMID:Interleukin-6 regulation of matrix metalloproteinase (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase (TIMP-1) expression in malignant non-Hodgkin's lymphomas. 1047 38

A primary cell culture system was developed for the cells of lymphoid organ tissue of kuruma shrimp, Penaeus japonicus. Minced tissues of lymphoid organs were seeded and incubated at 30 degrees C in medium 199 supplemented with 20% foetal bovine serum, a salt mixture and a lactalbumin hydrolysate (0.1 g/l). Fibroblast-like cells and epithelioid-like cells survived for 54 days. Cells did not survive after trypsin, collagenase or hyaluronidase treatment used for cell dissociation. Mitogens (Con A, PHA-P, Pokeweed) and insulin did not enhance cell proliferation. When penaeid rod-shaped DNA virus (PRDV) was inoculated into the lymphoid organ cell culture, a cytopathic effect was observed within 8 days. On the other hand, large granular haemocytes that were fractionated using a Percoll continuous density gradient were not infected with PRDV in vitro within 10 days, which was the longest period of haemocyte maintenance.
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PMID:Primary culture of lymphoid organ cells and haemocytes of kuruma shrimp, Penaeus japonicus. 1062 78

To investigate morphological changes occurring during cutaneous photoageing, a correlation between the number of infiltrating cells in the dermis and the degree of collagen damage was examined using sections from clinically normal chronically sun-exposed and sun-protected skin of Japanese female subjects. Haematoxylin and eosin-stained sections from 134 sun-exposed (subjects aged 3-82 years) and 73 sun-protected (subjects aged 1-86 years) areas demonstrated a predominant lymphoid cell and to a lesser extent histiocyte infiltration. The mean +/- SD number of lymphoid cells and histiocytes in the sun-exposed skin sections (427.0+/-192.2 and 147.8+/-83.3 cells/mm2, respectively) was significantly higher than in the sun-protected skin sections (292.6+/-98.3 and 125.9+/-59.0 cells/mm2, respectively) (P < 0.001 and P < 0.05, respectively), and the number of lymphoid cells in the sun-exposed skin sections increased significantly with age up to 50 years (r = 0.400, P < 0.001). Sun-exposed skin sections with severe collagen degeneration had a significantly higher number of lymphoid cells than those with slightly degenerated collagen (mean 626.3 vs. 482.4 cells/mm2, P < 0.01). The mean count of mast cells in sun-exposed skin was 202.0 cells/mm2; this did not vary with the age of the subjects or the level of collagen damage. Immunohistochemical studies using 24 frozen sections identified most of the lymphoid cells infiltrating sun-exposed skin as memory T lymphocytes (CD3+, CD4+ and CD45RO+). The number of cells which displayed immunoreactivity to matrix metalloproteinase (MMP)-1 in the sun-exposed skin sections was significantly higher than in the sun-protected skin sections (mean 170.2 vs. 113.6 cells/mm2, P < 0.05). Among these cells were observed CD3 and MMP-1 double-stained T lymphocytes, and T lymphocytes contacting MMP-1-positive cells. These morphological observations suggest that T lymphocytes infiltrating photodamaged skin may play a part in the degeneration and reduction of collagen through MMP-1 activity.
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PMID:Histological increase in inflammatory infiltrate in sun-exposed skin of female subjects: the possible involvement of matrix metalloproteinase-1 produced by inflammatory infiltrate on collagen degradation. 1073 Jul 59

Tissue inhibitor of metalloproteinases (TIMP)-1 and TIMP-2 are proteins with proteinase-inhibiting and cytokine properties. TIMP-1 is active primarily in B cells and B-cell lymphomas, whereas TIMP-2 expression is restricted to T cells. The expression of TIMP-1 and TIMP-2 in lymph nodes from patients with Hodgkin disease (HD) and in Hodgkin-derived cell lines was investigated. In situ hybridization showed TIMP-1 RNA expression in 3% to 80% of Hodgkin/Reed-Sternberg (H/R-S) cells from 14 of 15 patients, with results in one patient being at the lowest detection limit; no expression of TIMP-2 in H/R-S cells; and only weak expression of TIMP-2 in reactive lymphoid tissue. Production of TIMP-1 protein by H/R-S cells was accordingly found on immunohistochemical analysis of lymph nodes from patients with HD. There was only low expression of matrix metalloproteinase (MMP)-2, which is mainly inhibited by TIMP-2; no expression of MMP-1 and MMP-3 in reactive lymphoid tissue; and no expression of these MMPs in H/R-S cells. Thus, TIMP-1 expression in lymph nodes was not correlated with metalloproteinase expression. Five of 7 Hodgkin-derived cell lines expressed TIMP-1 at the protein level. Only one of these cell lines expressed TIMP-2, at the lowest detection limit. TIMP-1 levels in plasma from patients with HD were within the same range as those in plasma from healthy controls. Recombinant human TIMP-1 inhibited induced cell death in Hodgkin-derived cell lines in vitro. TIMP-1 and TIMP-2 inhibited T-cell cytotoxicity against autologous cells presenting tumor-associated antigens and in allogeneic mixed lymphocyte cultures. Thus, TIMP-1, aside from its role in proteinase equilibrium, is an autocrine and paracrine survival factor for H/R-S cells and an immunosuppressive protein expressed in Hodgkin lymphomas.
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PMID:Tissue inhibitor of metalloproteinases 1 is an autocrine and paracrine survival factor, with additional immune-regulatory functions, expressed by Hodgkin/Reed-Sternberg cells. 1175 80

Liver dendritic cells (DC) are believed to play important roles in liver immunity, autoimmunity, and in the regulation of hepatic allograft acceptance. However, limited information is available on the phenotypes and functions of DC in the liver. To address this issue, we isolated DC from murine liver using procedures that do not involve collagenase, and characterized the freshly isolated DC population that had not been subjected to in vitro expansion. Thence, based on the expression of CD4, B220, and CD11b, four subsets or groups of hepatic NK1.1(-)CD11c(+) DC were identified with the following phenotypes: B220(+)CD4(+), B220(+)CD4(-), B220(-)CD11b(+), and B220(-)CD11b(-). Each subset was further characterized both phenotypically and functionally. In addition to unique phenotypic expression, each subset displayed different allostimulation capability in mixed lymphocyte reaction assays. All four groups developed DC morphology following in vitro culture with activation agents and synthesized distinct patterns of cytokines in response to different stimuli. Taken together, our results suggest that groups I and II are IFN-alpha-producing plasmacytoid DC, group III cells are myeloid-related DC, while group IV is a heterogeneous population containing both myeloid- and lymphoid-related DC. Our results demonstrate the highly heterogeneous nature of hepatic DC, which is in agreement with the unique requirements for APC in the complex liver environment.
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PMID:Heterogeneity of dendritic cells in the mouse liver: identification and characterization of four distinct populations. 1259 54

Gastrointestinal tract associated lymphoid tissue is considered to be the main replication site for enteroviruses. In order to invade tissues to reach pancreatic islets, cardiac muscles, and other secondary replication sites, the virus has to survive circulation in the blood and find a way to get through endothelial cells. In the present study, the susceptibility of human endothelial cells to infections caused by human parechovirus 1 and several prototype strains of enteroviruses, representing different species (human poliovirus, human enterovirus B and C), and acting through different receptor families was examined. Primary endothelial cells isolated from human umbilical vein by collagenase perfusion and also an established human endothelial cell line, HUVEC, were used. Primary endothelial cells were highly susceptible to several serotypes of enteroviruses (coxsackievirus A13, echoviruses 6, 7, 11, 30, and poliovirus 1). However, coxsackievirus A 9 and echovirus 1 infected only a few individual cells while human parechovirus 1 and coxsackie B viruses did not show evidence of replication in primary endothelial cells. In general, primary endothelial cells were more sensitive to infection-induced cytolytic effect than HUVEC. Activation of endothelial cells by interleukin-1beta did not change the pattern of enterovirus infection. Immunofluorescence stainings of infected primary endothelial cells showed that expression of activation markers, E-selectin, and intercellular adhesion molecule-1, was clearly increased by several virus infections and the former molecule also by exposing cells to UV-light inactivated coxsackieviruses. In contrast, human leukocyte antigen-DR expression was not increased by virus infection.
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PMID:Enterovirus infection and activation of human umbilical vein endothelial cells. 1276 7

We produced two novel rat monoclonal antibodies (LA102 and LA5) to identify mouse lymphatic vessels and blood vessels, respectively. We characterized the two antibodies as to the morphological and functional specificities of endothelial cells of both types of vessels. The antibodies were produced by a rapid differential immunization of DA rats with collagenase- and neuraminidase-treated mouse lymphangioma tissues. LA102 specifically reacted with mouse lymphatic vessels except the thoracic duct and the marginal sinus of lymph nodes, but not with any blood vessels. In contrast, LA5 reacted with most mouse blood vessels with a few exceptions, but not with lymphatics. LA102 recognized a protein of 25-27 kDa, whereas LA5 recognized a molecule of 12-13 kDa. Neither antibody recognized any currently identified lymphatic or vascular endothelial cell antigens. Immunoelectron microscopy revealed that the antigens recognized by LA102 and LA5 were localized on both luminal and abluminal endothelial cell membranes of each vessel type. Interestingly, LA102 immunoreactivity was strongly expressed on pinocytic or transport vesicle membrane in the cytoplasm of lymphatic endothelium. Besides endothelial cells, both antibodies also recognized some types of lymphoid cells. Since, the LA102 antigen molecule is expressed on some lymphoid cells, it may play important roles in the migration of lymphoid cells and in some transport mechanisms through lymphatic endothelial cells.
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PMID:Production of two novel monoclonal antibodies that distinguish mouse lymphatic and blood vascular endothelial cells. 1668 12

Adoptive transfer of adjuvant-induced arthritis was used in this study to examine local macrophages and dendritic cells (DCs) during T cell-mediated synovial inflammation. We studied the influx of CD11b+CD11c+ putative myeloid DCs and other non-lymphoid CD45+ cells into synovium-rich tissues (SRTs) of the affected hind paws in response to a pulse of autoreactive thoracic duct cells. Cells were prepared from the SRTs using a collagenase perfusion-digestion technique, thus allowing enumeration and phenotypic analysis by flow cytometry. Numbers of CD45+ cells increased during the first 6 days, with increases in CD45+MHC (major histocompatibility complex) II+ monocyte-like cells from as early as day 3 after transfer. In contrast, typical MHC II(-) monocytes, mainly of the CD4(-) subset, did not increase until 12 to 14 days after cell transfer, coinciding with the main influx of polymorphonuclear cells. By day 14, CD45+MHC IIhi cells constituted approximately half of all CD45+ cells in SRT. Most of the MHC IIhi cells expressed CD11c and CD11b and represented putative myeloid DCs, whereas only approximately 20% were CD163+ macrophages. Less than 5% of the MHC IIhi cells in inflamed SRT were CD11b(-), setting a maximum for any influx of plasmacytoid DCs. Of the putative myeloid DCs, a third expressed CD4 and both the CD4+ and the CD4(-) subsets expressed the co-stimulatory molecule CD172a. Early accumulation of MHC IIhiCD11c+ monocyte-like cells during the early phase of T cell-mediated inflammation, relative to typical MHC II(-) blood monocytes, suggests that recruited monocytes differentiate rapidly toward the DC lineage at this stage in the disease process. However, it is possible also that the MHC IIhiCD11c+ cells originate from a specific subset of DC-like circulating mononuclear cells.
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PMID:Recruitment of dendritic cells and macrophages during T cell-mediated synovial inflammation. 1802 48

Murine gammaherpesvirus 68 (MHV-68) is a natural pathogen of rodents closely related to the human gammaherpesviruses Kaposi's sarcoma-associated herpesvirus and EBV. Following intranasal infection, the virus replicates in the lung epithelium prior to establishing latent infection in lymphoid tissue. Infection of mice deficient in IFN-gammaR signaling (IFN-gammaR-/-) results in a multiple organ fibrosis, in which the spleen is severely affected. We show here that by Day 12 postinfection, prior to development of fibrosis in the spleens of IFN-gammaR-/- mice, different subsets of splenic macrophages (Mvarphis) are morphologically activated and enter latently infected germinal centers (GCs). Mvarphis coexpressing arginase I (ARG1), a marker of alternative activation of Mvarphis, and murine Mvarphi markers F4/80, ER-TR9, and MOMA-1 are found in GCs of IFN-gammaR-/- mice but not of wild-type mice. Quantitative RT-PCR of spleen RNA confirms induction of ARG1 and in addition, shows up-regulation of found in inflammatory zone 1/resistin-like molecule-alpha, tissue inhibitor of metalloproteinase-1, matrix metalloproteinase-12, fibronectin, and factor XIIIA in IFN-gammaR-/- mice. In contrast, inducible NO synthase, associated with classical Mvarphi activation, is up-regulated following infection of wild-type mice but not IFN-gammaR(-/-) mice. Concomitant with the aaMvarphis, transcription of the Th2 cytokines IL-13, IL-21, and IL-5 is up-regulated. Thus, in the absence of IFN-gammaR signaling, MHV-68 initiates a Th2 immune response, leading to alternative activation of macrophages and induction of fibrosis. This system provides an important model for studying the pathogenesis of fibrosis initiated by a latent herpesvirus infection.
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PMID:Murine gammaherpesvirus-induced fibrosis is associated with the development of alternatively activated macrophages. 1843 82


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