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)

In the present study, we sought to identify the T cell-replacing factor which selectively induces IgG2b antibody formation in lipopolysaccharide-activated mouse spleen cells in vitro and in vivo, and which is present in the synovial fluid (SF) of rheumatoid arthritis (RA) patients. The protein A plaque assay was used to measure IgM, IgG1, IgG2b, and IgG3 plaque-forming cells. An enzyme-linked immunosorbent assay was used to measure interleukin-6 (IL-6) levels in RA SF. We found that IgG2b induction by RA SF is not caused by IL-6, IL-1, or any other inflammatory cytokines or mediators, such as transforming growth factor beta, platelet-derived growth factor, nerve growth factor, fibroblast growth factor, epidermal growth factor, elastase, collagenase, and phospholipase A2. IgG2b-inducing factor in RA SF has unique biological properties compared with those of the interleukins and inflammatory mediators known to be present in RA SF.
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PMID:Relationship between IgG2b-inducing activity in rheumatoid arthritis synovial fluid and other well-known cytokines and inflammatory mediators. 195 23

The roles of polypeptide growth factors in promoting wound healing and in directing the specificity and sequence of responses of different tissues in wounds are little understood. We investigated the influence of four growth factors on the rates of healing of a novel full thickness dermal ulcer placed on an avascular base in the rabbit ear. The wound model precludes significant wound contraction and requires new granulation tissue and epithelial cells for healing to originate centripetally. 5 micrograms (7-31 pmol/mm2) of platelet-derived growth factor-B chain (PDGF-BB), basic fibroblast growth factor (bFGF), and epidermal growth factor (EGF) applied locally at the time of wounding resulted in a twofold increase in complete reepithelialization of treated wounds (PDGF-BB, P = 0.02 chi square analysis; bFGF, P = 0.04; EGF, P = 0.05); transforming growth factor (TGF)-beta 1 significantly inhibited reepithelialization (P = 0.05). Both PDGF-BB and TGF-beta 1 uniquely increased the depth and area of new granulation tissue (P less than 0.005), the influx of fibroblasts, and the deposition of new matrix into wounds. Explants from 7-d old PDGF-BB-treated wounds remained metabolically far more active than controls, incorporating 473% more [3H]thymidine into DNA (P = 0.05) and significantly more [3H]leucine and [3H]proline into collagenase-sensitive protein (P = 0.04). The results establish that polypeptide growth factors have significant and selective positive influences on healing of full thickness ulcers in the rabbit.
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PMID:Growth factor-induced acceleration of tissue repair through direct and inductive activities in a rabbit dermal ulcer model. 199 53

The v-sis oncogene of simian sarcoma virus encodes a protein which is homologous to the human platelet-derived growth factor B-chain. The v-sis protein undergoes a series of processing steps including dimer formation and proteolytic digestion to generate several molecular sizes of the protein. Two of these v-sis proteins were expressed alone or as polyhedrin-sis fusion proteins using the Bombyx mori nuclear polyhedrosis virus vector. The polyhedrin-sis fusion proteins contained a collagenase-sensitive site at the junction. The expression levels of the fusion proteins whose polyhedrin portions consisted of only 8 amino-terminal amino acids were 3-4 times higher than those of non-fusion proteins. One of these fusion proteins was expressed in silkworm larvae and the v-sis protein was isolated from the fusion protein by collagenolysis followed by chromatography. Because the purified v-sis protein exhibited the same molecular size on SDS-polyacrylamide gels under reducing and non-reducing conditions, it was concluded to be monomeric in structure. It possessed chemotactic activity but lacked mitogenic activity. In addition, a small amount (approximately 1%) of monomeric v-sis protein was converted in vitro to the mitogenically active v-sis protein, which could be a homo-dimer.
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PMID:Characterization of v-sis protein expressed in silkworm larvae using the Bombyx mori nuclear polyhedrosis virus vector. 201 72

Recombinant human interleukin-1 alpha (IL-1 alpha) induced a time-dependent (0-72 hours) and concentration-dependent (0.01-10 ng/ml) production of metalloproteinases (collagenase, gelatinase, stromelysin) and prostaglandin E2 (PGE2) in rabbit articular chondrocytes (RAC). Exposure of RAC to recombinant human platelet-derived growth factor homodimer BB (PDGF-BB; 2-200 ng/ml) in the presence of stimulatory and substimulatory concentrations of IL-1 alpha resulted in a marked augmentation of metalloproteinase and PGE2 production. PDGF-BB exerted no agonist effects on RAC responsiveness. PDGF-BB up-regulated the number of IL-1 receptors per chondrocyte but had no effect on receptor affinity. Cycloheximide and actinomycin D caused a concentration-dependent suppression of the PDGF-BB-mediated potentiation of radiolabeled IL-1 alpha binding to RAC and cell responsiveness to IL-1 alpha. Similarly, IL-1 increased the number of PDGF receptors on RAC without changing receptor affinity. These data are discussed within the context of cytokine-growth factor interactions as components of the pathogenesis of arthritic diseases.
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PMID:Platelet-derived growth factor potentiates cellular responses of articular chondrocytes to interleukin-1. 205 15

Endothelial cells play a fundamental role in the pathogenesis of chronic inflammatory arthritis in humans such as rheumatoid arthritis (RA), as well as experimental animal models such as streptococcal cell wall (SCW) arthritis in Lewis (LEW/N) rats. This review summarizes data in support of this concept. The earliest apparent abnormalities in synovial tissues of patients with RA and Lewis rats with SCW arthritis appear to reflect microvascular endothelial cell activation or injury. At the molecular level, the abnormalities include enhanced expression by endothelial cells of activation markers such as class II major histocompatibility complex antigens, phosphotyrosine, leukocyte adhesion molecules, oncoproteins such as c-Fos and c-Myc, and metalloproteinases such as collagenase and transin/stromelysin. The development of severe, chronic, destructive arthritis is dependent upon thymic-derived lymphocytes and is accompanied by tumorlike proliferation of cells in the synovial connective tissue stroma (blood vessels and fibroblastlike cells), which results in resorptive destruction of bone and cartilage. Multiple criteria support the analogy to a neoplastic process. Paracrine and autocrine factors such as interleukin-1 (IL-1), platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-beta), and heparin-binding fibroblast growth factors (HBGF, FGF) appear to play important roles in the generation of these lesions. Finally, in addition to the autocrine and paracrine regulatory factors, neuroendocrine factors, particularly the hypothalamic-pituitary-adrenal axis, appear to be involved in the counterregulation of the inflammatory process. The counterregulatory effects are mediated, in part, by inhibition of endothelial cell activation by corticosteroids.
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PMID:Endothelial cells and the pathogenesis of rheumatoid arthritis in humans and streptococcal cell wall arthritis in Lewis rats. 205 44

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

In human foreskin fibroblast cultures, two proteins with Mr 60,000 and 55,000 were found to be induced about 3.5-fold by epidermal growth factor (EGF), platelet-derived growth factor, and beta-transforming growth factor. The induced proteins were identified as procollagenases by immunoprecipitation of induced medium with antibodies to purified human fibroblast collagenase. Collagenase enzyme activity in the medium from EGF-treated cultures was also induced at least 3-fold compared to control cultures. Induction of collagenase was dependent upon de novo protein and RNA synthesis and was observed in the medium 10 h after addition of EGF. Although these growth-promoting factors interact with separate membrane receptors, each induced the secretion of a common protein, suggesting that collagenase may be important in some aspect of mitogenesis, cell mobilization, and migration.
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PMID:Induction of collagenase secretion in human fibroblast cultures by growth promoting factors. 298 81

Patients with Werner's syndrome, an autosomal recessive disorder, undergo an accelerated aging process that leads to premature death. Fibroblasts from such patients typically grow poorly in culture. Here it is shown that fibroblasts from a patient with Werner's syndrome have a markedly attenuated mitogenic response to platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF). In contrast, they have a full mitogenic response to fetal bovine serum. Both PDGF binding and receptor numbers per cell are unaltered. The Werner's syndrome cells express high constitutive levels of collagenase in vitro. Although PDGF enhances collagenase expression through increased levels of hybridizable collagenase messenger RNA in normal skin fibroblasts, no induction of collagenase occurs in the Werner's syndrome fibroblasts. Moreover, the failure to respond to this agonist effect of PDGF is not restored by fetal bovine serum. The data suggest that failure of one or more PDGF-mediated pathways in Werner's syndrome cells may contribute to the phenotypic expression of the disorder.
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PMID:Diminished response of Werner's syndrome fibroblasts to growth factors PDGF and FGF. 302 82

It is proposed that interferon may be an active agent in the treatment of patients with idiopathic myelofibrosis. In this disorder the megakaryocyte cell lineage plays a major role in the deposition of bone marrow collagen by the release of growth promoting factors, including platelet-derived growth factor, which are mitogenic for fibroblast proliferation. Interferon reduces collagen deposition in the bone marrow by suppressing the activity of the proto-oncogene, which is involved in the production of growth factors from abnormal megakaryocytes and platelets. A direct myeloid cytoreductive effect of interferon upon the megakaryocyte proliferation contributes to reducing growth factor activity in the bone marrow. Finally, interferon induces monocytoid differentiation, thereby increasing bone marrow collagenase-activity. Thus, interferon has several actions, which in concert might reduce bone marrow collagen in myelofibrosis.
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PMID:Hypothesis: a possible role for interferon in the treatment of idiopathic myelofibrosis. 322 65

Cementum forms the interface between root dentin and periodontal ligament through which periodontal connective tissue is attached to root surfaces. We have examined how cementum components influence the biological activities of gingival fibroblasts. Cementum was harvested from freshly extracted human teeth and extracted sequentially with 0.5 mol/L acetic acid, 4 mol/L guanidine-0.5 mol/L EDTA, and bacterial collagenase. The extracts were concentrated and analyzed for mitogenic activity to human gingival fibroblasts. DNA synthesis was assayed by measurement of [3H]thymidine incorporation by quiescent fibroblasts activated to divide, and cell growth was determined by the counting of cells over a 10-day period. Results showed that extracts of cementum stimulated quiescent gingival fibroblasts to synthesize DNA and grow. The stimulation was dose-dependent, and most of the stimulatory activity was extracted by acid. Addition of small quantities of serum potentiated the mitogenic activity to levels greater than those of control cultures containing 10% fetal calf serum. The mitogenic activity was heat-stable, but it was destroyed by trypsin. Neither platelet-derived growth factor (PDGF) nor epidermal growth factor (EGF) was detectable in the cementum extract, and extracts of human dentin and skin contained very little mitogenic activity. We conclude that cementum contains substances capable of regulating the growth of gingival fibroblasts, and that these substances may play an important role in gingival connective tissue formation and regeneration.
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PMID:Mitogenic activity of cementum components to gingival fibroblasts. 347 10


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