Improved gelatinase a selectivity by novel zinc binding groups containing galardin derivatives

Augé, Franck; Hornebeck, William; Decarme, Martine; Laronze, Jean‐Yves

doi:10.1016/s0960-894x(03)00214-2

Cited by 71 publications

(37 citation statements)

References 20 publications

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“…Consistent with this finding, the amount of fluorescent material released into the culture supernatant was higher (B1.7-fold) in R À cells than in wt or R þ cells (Figure 6c). This increase was largely suppressed when the cells were treated with either a broadspectrum synthetic MMP inhibitor GM6001 (GM) (Auge et al, 2003) or an endogenous MMP inhibitor, TIMP-1 (TP1) or TIMP-2 (TP2) (Nagase et al, 2006) (Figure 6d). Hence, the elevated gelatinolytic activity in R À cells is likely to represent deregulated MMPs.…”

Section: Fak Rho Family Small Gtpases and Detyrosinated Tubulin In Rmentioning

confidence: 99%

The membrane-anchored metalloproteinase regulator RECK stabilizes focal adhesions and anterior–posterior polarity in fibroblasts

et al. 2009

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Accumulating evidence indicates that Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a membrane-anchored matrix metalloproteinase regulator, plays crucial roles in mammalian development and tumor suppression. Its mechanisms of action at the single cell level, however, remain largely unknown. In mouse fibroblasts, RECK is abundant around the perinuclear region, membrane ruffles and cell surface. Cells lacking Reck show decreased spreading, ambiguous anteriorposterior (AP) polarity, and increased speed and decreased directional persistence in migration; these characteristics are also found in transformed fibroblasts and fibrosarcoma cells with low RECK expression. RECK-deficient cells fail to form discrete focal adhesions, have increased levels of GTP-bound Rac1 and Cdc42, and a marked decrease in the level of detyrosinated tubulin, a hallmark of stabilized microtubules. RECK-deficient cells also show elevated gelatinolytic activity and decreased fibronectin fibrils. The phenotype of RECK-deficient cells is largely suppressed when the cells are plated on fibronectin-coated substrates. These findings suggest that RECK regulates pericellular extracellular matrix degradation, thereby allowing the cells to form proper cell-substrate adhesions and to maintain AP polarity during migration; this mechanism is compromised in malignant cells.

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Section: Fak Rho Family Small Gtpases and Detyrosinated Tubulin In Rmentioning

confidence: 99%

The membrane-anchored metalloproteinase regulator RECK stabilizes focal adhesions and anterior–posterior polarity in fibroblasts

et al. 2009

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“…11,12 Similar to CHX, galardin as a synthetic inhibitor of MMP-1, À2, À3, À8, and À9 is acting as a zinc chelator. 13 Green tea catechins, mainly epigallocatechin-gallate (EGCG), change the secondary structure of collagenases by hydrogen bonding and hydrophobic interactions. 14 As well, binding of metal ions might cause conformational changes that inactivate their catalytic function.…”

Section: Introductionmentioning

confidence: 99%

Effect of Different Matrix Metalloproteinase Inhibitors on Microtensile Bond Strength of an Etch-and-Rinse and a Self-etching Adhesive to Dentin

Pei

Zaruba

Attin

et al. 2015

Operative Dentistry

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Matrix metalloproteinase (MMP) inhibitors prevented bond strength loss of an etch-andrinse adhesive over time. Bond strength of a self-etching adhesive was not significantly reduced with 9 months of aging; thus, MMP inhibitors did not show a significant effect. SUMMARY Aim:This study aimed to analyze the effect of different matrix metalloproteinase (MMP) inhibitors on the microtensile bond strength (microTBS) of an etch-and-rinse and a selfetching adhesive after 9 months of aging.Methods and Materials: Flat human dentin surfaces were bonded either with an etch-andrinse adhesive (Optibond FL) or a self-etching adhesive (Clearfil SE Bond). Dentin surfaces were left untreated or were pretreated with MMP inhibitors (2% chlorhexidine digluconate [CHX], 0.05% green tea extract, 1 mM ferrous sulfate, or 0.2 mM galardin) prior to application of the adhesive. Composite buildups were made incrementally. Pretreated groups were tested after 9 months of storage in artificial saliva (378C) and compared with untreated groups, which were tested immediately (initial microTBS) and upon aging (9-month microTBS). Data were analyzed by linear mixedmodel regression. Failure mode analysis was performed microscopically and statistically analyzed by repeated-measures analysis of variance (p,0.05).

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“…Many of synthetic compounds, which mainly categorized into a zinc-binding group and a peptide-mimic group, act as competitive inhibitors against MMP activity (3,(28)(29)(30)(31). In contrast, many of naturally-occurring substances that can control MMP activity have a diversity in the structure including steroids, flavonoids, rotenoids, and terpenoids, and suppress expression of MMP gene by a regulation of signal transduction in cells (32)(33)(34)(35)(36).…”

Section: Resultsmentioning

confidence: 99%

An aqueous extract from toad skin prevents gelatinase activities derived from fetal serum albumin and serum-free culture medium of human breast carcinoma MDA-MB-231 cells

Nakata

Kawaguchi

Oikawa

et al. 2015

DD&T

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Improved gelatinase a selectivity by novel zinc binding groups containing galardin derivatives

Cited by 71 publications

References 20 publications

The membrane-anchored metalloproteinase regulator RECK stabilizes focal adhesions and anterior–posterior polarity in fibroblasts

The membrane-anchored metalloproteinase regulator RECK stabilizes focal adhesions and anterior–posterior polarity in fibroblasts

Effect of Different Matrix Metalloproteinase Inhibitors on Microtensile Bond Strength of an Etch-and-Rinse and a Self-etching Adhesive to Dentin

An aqueous extract from toad skin prevents gelatinase activities derived from fetal serum albumin and serum-free culture medium of human breast carcinoma MDA-MB-231 cells

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