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)

Previous studies have described a 22 kD IL-1 inhibitor in the supernatant of human monocytes cultured on adherent immune complexes (J. Immunol. 134:3868, 1985). The studies reported herein further detail the conditions of production and biological properties of this IL-1 inhibitor. The inhibitor was produced by human monocytes cultured on adherent human IgG with maximal production between 8 and 24 hr. The IL-1 inhibitor was not performed in the cells but required transcription and new protein synthesis. The inhibitor blocked IL-1 augmentation of PHA-induced murine thymocyte proliferation but not IL-2-induced stimulation of CTLL or HT-2 cell lines. In addition, the inhibitor blocked IL-1-stimulated collagenase production from rabbit articular chondrocytes and IL-1-induced PGE2 production from human fibroblasts and synovial cells. The IL-1 inhibitor was not transforming growth factor beta (TGF beta) as determined by: the failure of anti-TGF beta antibodies to reduce IL-1 inhibitory activity, the separation of TGF beta from the IL-1 inhibitor by ion exchange chromatography, and the failure of TGF beta to inhibit IL-1-induced PGE2 production from synovial cells. IL-1 and the inhibitor showed no immunological cross-reactivity by Western blot analysis. The inhibitor specifically blocked binding of IL-1 to its receptor on the murine thymoma cell line EL4-6.1. These results indicate that a specific inhibitor of IL-1-induced immune and inflammatory cell responses is produced by monocytes cultured on adherent immune complexes or adherent IgG. This IL-1 inhibitor may be of importance in modulating the effects of IL-1 in the monocyte microenvironment.
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PMID:An IL-1 inhibitor from human monocytes. Production and characterization of biologic properties. 252 82

IL-1 and prostaglandin (PGE2, PGF2 alpha, TXB2) concentrations, PLA2 activity, neutral protease activity, and collagenase activity specific for types I and II collagen were determined in the SF of patients suffering from RA, before and after treatment with TA. Active and latent forms of protease and collagenases were regularly detected but were unrelated to IL-1, PLA2, and PGE2. TA induced a significant decrease in tested eicosanoids but IL-1, PLA2, and proteases were unchanged.
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PMID:Effects of tiaprofenic acid on interleukin 1, phospholipase A2 activity, prostaglandins, neutral protease, and collagenase activity in rheumatoid synovial fluid. 254 31

We show that platelet-derived growth factor (PDGF) and IL-1 interact in both a synergistic and antagonistic manner to regulate synovial fibroblast-like cells (synoviocytes) derived from patients with rheumatoid arthritis. PDGF and IL-1 operated synergistically in vitro to stimulate synoviocyte proliferation in the presence of indomethacin. However, when these same cells were treated with PDGF and IL-1 in the absence of indomethacin, IL-1 inhibited PDGF-stimulated synoviocyte proliferation. Moreover, exogenous PGE2, a PG known to be produced in response to IL-1, dramatically inhibited synoviocyte proliferation induced by PDGF. PDGF also acted synergistically to markedly increase production of PGE2 stimulated by IL-1. This is in contrast to the antagonistic effect PDGF had on IL-1-stimulated collagenase transcription. IL-1 stimulated collagenase transcription, but PDGF did not. It in fact inhibited IL-1 stimulation of collagenase gene expression. These data differ somewhat from those reported for dermal fibroblasts. Our data further indicate that the effects of cytokines vary from one cell type to another, even amongst "fibroblasts," and illustrate the complexity of cytokine regulation of rheumatoid synoviocyte function.
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PMID:Platelet-derived growth factor and IL-1 interactions in rheumatoid arthritis. Regulation of synoviocyte proliferation, prostaglandin production, and collagenase transcription. 254 78

Human osteoblast cultures (hOB) were examined for the production of interstitial collagenase, tissue inhibitor of metalloproteinases (TIMP), and gelatinolytic enzymes. Cells were isolated by bacterial collagenase digestion of trabecular bone (vertebra, rib, tibia, and femur) from 11 subjects (neonatal to adult). Confluent cultures were exposed to phorbol 12-myristate 13-acetate, PTH, PGE2, epidermal growth factor, 1,25(OH)2 vitamin D3, recombinant human IL-1 beta, and dexamethasone. Collagenase and TIMP were assayed immunologically and also by measurements of functional activity. Collagenase was not secreted in significant quantities by human bone cells under any tested condition. Furthermore, collagenase mRNA could not be detected in hOB. However, hOB spontaneously secreted large amounts of TIMP for at least 72 h in culture. hOB TIMP was found to be identical to human fibroblast TIMP by double immunodiffusion, metabolic labeling and immunoprecipitation, Northern blot analysis, and stoichiometry of collagenase inhibition. SDS-substrate gel electrophoresis of hOB-conditioned media revealed a prominent band of gelatinolytic activity at 68 kD, and specific polyclonal antisera established its identity with the major gelatinolytic protease of human fibroblasts. Abundant secretion of gelatinolytic, but not collagenolytic, enzymes by hOB may indicate that human osteoblasts do not initiate and direct the cleavage of osteoid collagen on the bone surface, but may participate in the preparation of the bone surface for osteoclast attachment by removal of denatured collagen peptides. The constitutive secretion of TIMP may function to regulate metalloproteinase activity.
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PMID:Human osteoblasts in vitro secrete tissue inhibitor of metalloproteinases and gelatinase but not interstitial collagenase as major cellular products. 254 36

Ro 23-6457, (all-E)-3,7-dimethyl-9-[2-(trifluoromethyl)-6-(nonyloxy)phenyl]-2, 4,6,8- nonatetraenoic acid, and Ro 23-2895, (all-E)-9-[2-(nonyloxy)phenyl]-3,7-dimethyl-2,4,6,8-nonatetraen oic acid, are two novel retinoid analogs which exhibit antiinflammatory activity in both the developing and the established rat adjuvant arthritis models [8]. Here we investigated the effect of these two compounds on the production of arachidonic acid (AA) metabolites in two in vitro test systems [i.e., Ca2+ ionophore A23187 (I)-stimulated resident rat peritoneal macrophages (MO) and cytokine-stimulated human dermal fibroblasts (HDF)]. Both compounds, Ro 23-6457 and Ro 23-2895, significantly inhibited the release of 14C-AA metabolites and the production of LTB4, PGE2, and 6-keto-PGF1 alpha in I-stimulated MO, at concentrations of 1-33 microM. Both compounds also inhibited the production of PGE2 in HDF stimulated by either rhuIL-1 alpha or huTNF alpha at concentrations of 1 x 10(-5) to 1 x 10(-7) M. Ro 23-2895 was also a potent inhibitor of IL-1-induced collagenase production in rheumatoid synovial cells (IC50 approximately 1 to 2.5 x 10(-8) M). The inhibitory profile of these novel compounds in these cell systems is therefore similar to that of other known antiinflammatory retinoids (e.g., all-trans- and 13-cis-retinoic acid). Inhibitory effects such as those described here might in part contribute to the antiinflammatory activity of these compounds in vivo.
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PMID:In vitro inhibition of arachidonic acid metabolism by two novel retinoid analogs. 255 63

Prostaglandin (PG) inhibits the hydroosmotic effect of vasopressin. We therefore reexamined the interaction of vasopressin (VP), cAMP, and prostaglandins in toad bladder epithelial cells. Vasopressin slightly, but reproducibly, stimulated PGE2 and thromboxane B2 (TXB2) synthesis in cells prepared by the use of collagenase. When cells were prepared in the presence of a readily reversible cyclooxygenase inhibitor, ibuprofen, subsequent PGE2 synthesis was enhanced sevenfold but that of TXB2 was not. Increasing cAMP by either phosphodiesterase inhibition or 8-bromo-cAMP significantly inhibited both basal and VP-stimulated PGE2 synthesis. This inhibition was overcome by addition of arachidonic acid. Future studies employing these agents will have to consider these effects. VP enhanced 32P labeling of phosphatidylinositol (PI) and phosphatidic acid. This effect was prevented by the phosphodiesterase inhibitor, which also decreased phosphatidylcholine labeling. The results indicate that the phosphodiesterase inhibitor for cAMP may decrease PG formation by interfering with phospholipase activation. Furthermore, VP, similar to its effect in the liver, also increases PI turnover in toad bladder. This may initiate PG synthesis and provide a link among VP, cAMP, and calcium. A double-reciprocal feedback is proposed, whereby VP stimulates PG synthesis in a cAMP-independent manner and also inhibits PG synthesis in a cAMP-dependent manner.
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PMID:Interactions of vasopressin, cAMP, and prostaglandins in toad urinary bladder. 257 84

The osteoblast phenotype is characterized by its ability to (a) synthesize a well defined mineralized collagenous matrix, (b) regulate the remodeling process by synthesizing local hormones (PGE2) and specific molecules (osteocalcin) and enzymes (alkaline phosphatase and collagenase), (c) respond to a variety of hormones (PTH, PGs, vitamin-D metabolites, steroids and growth factors), (d) respond to mechanical stimulation. Most of osteoblast culture systems meet many of the above qualifications though most fail to show the PTH effect on DNA synthesis, (c), and mechanical stimulation (d). Here we show that by using trypsin digestion and serum-containing low calcium medium (0.25 mM), all the above listed osteoblast phenotypic characteristics are demonstrated including their responsiveness to mechanical stimulation and the PTH effect on DNA synthesis.
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PMID:Calvaria derived osteogenic cells: phenotypic expression in culture. 261 64

It has been proposed that bacteria in infected root canals are most important agents to pathogenesis of the periapical lesion. The aim of the present study was to examine the roles of macrophage on the mechanism of development of periapical lesion. Therefore the influences of bacteria isolated from infected root canals to macrophage functions and the effects of products from macrophage stimulated with bacterial components to periodontal tissue were investigated. In this study, sonic extracts prepared from Bacteroides buccae predominantly isolated from root canals were tested for its capacity of induction of chemotaxis and production of prostaglandin E2 and collagenase from human peripheral monocyte. Furthermore prostaglandin E2, collagenase production and alkaline phosphatase activity of fibroblasts from human periodontal ligament (HPLF), pulp (HPF) and gingiva (Gin 1) stimulated with macrophage conditioned medium (MCM) stimulated with B. buccae sonic extracts were examined. The results obtained were as follows. The sonic extract of B. buccae showed capacity to induce macrophage chemotaxis directly and by activation of serum complement, and the serum activated with sonic extract of B. buccae was more active than the serum activated with LPS of Salmonella typhimurium. Prostaglandin E2 production of macrophage was increased when the cells were stimulated by sonic extracts of B. buccae, but collagenase activity. toas not increased. MCM stimulated with sonic extracts of B. buccae fot 48 hours strongly induced PGE2 and collagenase production from HPLF and HPF, at the same time sonic extract showed the similar capacity of induction of the PGE2 production of MCM. But, HPF stimulated with sonic extract showed the low activity of induction of the PGE2 production. On the other hand, Gin 1 cell produced a few amount of the PGE2 when it was stimulated with MCM, but not produced collagenase. Alkaline phosphatase activity of HPLF and HPF had been inhibited by addition of MCM stimulated with B. buccae sonic extract.
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PMID:[The roles of macrophage on the mechanism of development of periapical lesion. The response of macrophage stimulated with bacteria isolated from infected root canals]. 263 71

We have earlier shown that first trimester human decidual cells and decidual macrophages suppress T lymphocyte alloreactivity in an MHC-unrestricted manner by secreting PGE2, which blocks the generation of IL-2 receptors (IL-2R) and production of IL-2 by lymphocytes but does not interfere with the interaction between IL-2 and IL-2R or the lytic function of CTL, once generated. The present study examined whether these events constituted a physiological, immunoprotective mechanism in situ against the activation of maternal decidua-infiltrating leukocytes with potential anti-trophoblast cytocidal function. We examined (1) whether there was IL-2R expression, IL-2 production, or anti-trophoblast killer activity in short-term (0-3 day) cultures of collagenase-dispersed first trimester human decidua inclusive of leukocytes; (2) if not, whether any of these parameters could be stimulated in these cultures by blocking PGE2 synthesis with indomethacin, or neutralizing PGE2 with anti-PGE2 antibody; (3) whether exogenously added recombinant IL-2 in the presence or absence of indomethacin stimulated IL-2R expression or anti-trophoblast killer function in these cultures. IL-2R (as defined by Tac antigen) was measured in the whole cell population by a radioimmunoassay and further examined at the cellular level with radioautography. IL-2 production in culture supernatants was measured from the proliferative response (3HTdR uptake) of an IL-2-dependent (CTLL) cell line. Killer activity in fresh or cultured decidua-associated cells as well as PBL of normal or pregnant subjects was measured against 51Cr-labeled targets inclusive of autologous cytotrophoblast cells or long-term human trophoblast cell lines, K562 and Daudi cells. Results revealed a complete absence of IL-2R expression, IL-2 production, or anti-trophoblast killer activity in the untreated cultures of the decidua, but all these parameters were significantly stimulated in the presence of indomethacin or anti-PGE2 antibody. The indomethacin-stimulated killer cells had NK-like activity. Presence of high dose exogenous IL-2 alone in these cultures strongly stimulated IL-2R expression and anti-trophoblast killer function, which were augmented further in the additional presence of indomethacin. The resultant killer cells had LAK cell-like activity. These findings suggest that PGE2 secretion by first trimester human decidual cells blocks activation of maternal leukocytes in the decidua with potential anti-trophoblast killer function, by inhibiting IL-2 receptor generation and IL-2 production in situ.
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PMID:PGE2-mediated immunosuppression by first trimester human decidual cells blocks activation of maternal leukocytes in the decidua with potential anti-trophoblast activity. 278 22

Transforming growth factor alpha (TGF-alpha) and interleukin-1 (IL-1) have been shown to affect bone metabolism in vitro by prostaglandin-dependent and PG-independent mechanisms. We assessed the effects of the combination of these two agents on [3H]thymidine (TdR) incorporation into DNA, DNA content, [3H]proline incorporation into collagenase-digestible (CDP), noncollagen protein (NCP), and PGE2 production in 21 day fetal rat calvaria cultured for 24-96 h. We also determined whether TGF-alpha plus IL-1 altered procollagen mRNA levels at 96 h. TGF-alpha, 1-30 ng/ml, produced a 41-59% increase in TdR incorporation into DNA, but the effect was partially blocked by human recombinant IL-1. At 96 h TGF-alpha alone or in combination with IL-1 significantly increased the DNA content of calvaria. At 96 h, TGF-alpha inhibited CDP labeling and the addition of IL-1 further enhanced this inhibitory effect. The enhanced inhibitory effect of TGF-alpha plus IL-1 on collagen synthesis was associated with a synergistic increase in prostaglandin accumulation in the medium. Addition of indomethacin blocked PGE2 accumulation and partially reversed the inhibitory effect of TGF-alpha alone or in combination with IL-1 on collagen synthesis. TGF-alpha decreased procollagen mRNA levels by 55%, but the combination of TGF-alpha plus IL-1 decreased procollagen mRNA levels by 82%. Our results show that TGF-alpha and IL-1, which are both produced by certain tumors as well as activated macrophages, appear to act synergistically to increase prostaglandin synthesis and inhibit collagen synthesis in vitro. Thus these agents may have a regulatory role on bone formation in vivo.
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PMID:Effects of transforming growth factor alpha and interleukin-1 on DNA synthesis, collagen synthesis, procollagen mRNA levels, and prostaglandin E2 production in cultured fetal rat calvaria. 281 17


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