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The Action of Collagenase on Synthetic Peptides ,

T1 - Enhanced synthesis of collagenase by human keratinocytes cultured on type I or type IV collagen

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Osteoblast collagenase: Collagenase synthesis by …

These findings provide insight into the intracellular events regulating monocyte collagenase synthesis and also implicate monocytes as a target of anti-inflammatory agents which ameliorate connective tissue degradation associated with chronic inflammatory lesions.

T1 - Particle-induced synthesis of collagenase by synovial fibroblasts

One way in which NSAIDs stop the chondrocytes from repairing themselves is by the inhibition of the synthesis of Prostaglandin E2 (PGE2). Prostaglandins (PG) are produced by most human cell types (including chondrocytes) and have a variety of physiologic functions. PG synthesis is initiated by the mobilization of arachidonic acid from cell membrane phospholipids as a result of the enzyme phospholipase A2. The enzyme cyclooxygenase along with other enzymes converts arachidonic acid to five primary prostaglandins: PGD2, PGE2, PGI2 (Prostacyclin), PGF2a, and TXA2 (thomboxane). (See Figure 13.) These PGs have a variety of functions including the mediation of inflammation, calcium movement, sensitization of spinal neurons to pain, blood clotting, blood pressure, circulation, control of blood flow in kidneys, hormone regulation, protection of gastrointestinal lining, and the control of cell growth.80, 81 Chondrocytes and synovial fibroblasts produce PGE2. PGE2 levels are increased to an impact load on articular cartilage or during cartilage degeneration.82, 83 PGE2 is reported to have anabolic effects on cartilage: increasing proteoglycan and DNA and collagen synthesis,84, 85 stimulating proliferation and proteoglycan aggrecan synthesis,86, 87 and, at low concentrations, stimulating type II collagen synthesis.88

Synthesis of collagenase inhibitor by KB cells - JST

Dexamethasone inhibited PGE2 synthesis, which resulted in the suppression of collagenase.

Dexamethasone, colchicine or retinoic acid all inhibited collagenase synthesis by monocytes in a dose-dependent manner although the effect of these drugs on monocyte PGE2 synthesis differed.

Additionally, dibutyryladenosine cyclic monophosphate (dBcAMP) restored collagenase synthesis in indomethacin-blocked cultures, indicating a PGE2-dependent generation of cAMP requirement for collagenase production similar to that demonstrated in experimental animals systems.

Enhanced synthesis of collagenase by human …

T1 - Induction of stromelysin-1 and collagenase synthesis in fibrochondrocytes by tumor necrosis factor-α

AB - We have recently demonstrated that human keratinocytes synthesize and secrete procollagenase and tissue inhibitor of metalloproteinases (TIMP) in culture. We have examined the response of keratinocyte collagenase production to the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), interleukin-1, extracellular matrix proteins and phagocytosis. Collagenase production in keratinocytes was markedly stimulated by TPA and paralleled the morphologic changes induced by the phorbol ester. Synthesis of collagenase increased six- to 34-fold with TPA, whereas the level of TIMP rose only three-fold. Interleukin-1 did not stimulate collagenase production by the keratinocytes, in contrast to its effect on cultured fibroblasts. When keratinocytes were plated on type I or type IV collagen, they synthesized increased amounts of collagenase compared with cells cultured on laminin or in the absence of matrix. TIMP synthesis was not increased by collagen. Finally, phagocytosis of latex beads did not augment collagenase production by the keratinocytes.

N2 - We have recently demonstrated that human keratinocytes synthesize and secrete procollagenase and tissue inhibitor of metalloproteinases (TIMP) in culture. We have examined the response of keratinocyte collagenase production to the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), interleukin-1, extracellular matrix proteins and phagocytosis. Collagenase production in keratinocytes was markedly stimulated by TPA and paralleled the morphologic changes induced by the phorbol ester. Synthesis of collagenase increased six- to 34-fold with TPA, whereas the level of TIMP rose only three-fold. Interleukin-1 did not stimulate collagenase production by the keratinocytes, in contrast to its effect on cultured fibroblasts. When keratinocytes were plated on type I or type IV collagen, they synthesized increased amounts of collagenase compared with cells cultured on laminin or in the absence of matrix. TIMP synthesis was not increased by collagen. Finally, phagocytosis of latex beads did not augment collagenase production by the keratinocytes.

Conversely, conditioned medium taken from unstimulated cultures contains an inhibitor of collagenase synthesis.
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  • What Is Transdermal Verapamil 15% Gel and How Does …

    T1 - Inducible synthesis of collagenase and other neutral metalloproteinases by cells of aortic origin

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    Cycloheximide blocks RA stimulation of collagenase mRNA, demonstrating the need for de novo protein synthesis.

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13/11/1997 · Results

We conclude that synovial fibroblasts regulate collagenase synthesis via an autocrine mechanism that includes the synthesis of both an inducer and inhibitor.

Evidence for pretranslational regulation

This protein, which has a Mr ∼ 20–25k by HPLC gel filtration antagonizes collagenase synthesis induced by phorbol esters, exogenous ll 1, and the autologous inducer.

Autoregulation of collagenase ..

Moreover, the synthetic heterotrimers were cleaved by interstitial collagenases in a single cut through all three chains without release of intermediates during the relatively slow enzymatic digestion process.

Bacterial Cellulose/Collagen Hydrogel for Wound Healing

Both proteins are active at nanomolar amounts and may function as polypeptide hormones in regulating collagenase synthesis and, hence, connective tissue remodeling.

Collagenase is an enzyme that breaks the peptide bonds of collagen.

Although the complex cystine knot of natural collagen was reduced in these synthetic heterotrimers to two interchain-disulfide bridges, it showed not only the expected entropic contribution to the refolding process by keeping the three chains assembled, but more importantly a triple-helix nucleation was induced.

Premature Rupture of the Fetal Membranes — NEJM

It is clear from the scientific literature that NSAIDs from in vitro and in vivo studies in both animals and humans have a significant negative effect on cartilage matrix which causes an acceleration of the deterioration of articular cartilage in osteoarthritic joints. The preponderance of evidence shows that NSAIDs have no beneficial effect on articular cartilage and accelerate the very disease for which they are most used and prescribed. While the rapid deterioration of joints after long-term NSAID treatment can be from a loss of proactive pain sensations, it is much more likely that it is a direct effect of NSAIDs on cartilage. (See Figure 18.) Some of these effects can be seen in Figure 19 and include inhibition of chondrocyte proliferation, synthesis of cellular matrix components, glycosaminoglycan synthesis, collagen synthesis, and proteoglycan synthesis. Clinically this is manifested as an accelerated progression of the knee or hip osteoarthritis as seen by standard radiographs. The long-term consequence of the deterioration of the joint is a need for joint replacement. This author notes that massive NSAID use in osteoarthritic patients since their introduction over the past forty years is one of the main causes of the rapid rise in the need for hip and knee replacements both now and in the near future.

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