Inhibition of transcription factor NF-κB reduces matrix metalloproteinase-1, -3 and -9 production by vascular smooth muscle cells

Bond, Mark; Chase, Alex; Baker, Andrew H.; Newby, Andrew C.

doi:10.1016/s0008-6363(01)00220-6

Cited by 332 publications

(237 citation statements)

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“…This phenomenon is closely similar to that observed in COPD patients and in mice with emphysema induced by cigarette smoke or gene knockout (23,(47)(48)(49)(50). Taking account of the fact that the promoter regions of the MMP2 and MMP9 genes contain binding sites for NF-B for their transcriptional regulation (8,9), the increased expression of MMP-2 and MMP-9 in Ig-Hepta Ϫ/Ϫ mice is likely to be mediated through ROS-dependent NF-B activation. Because MMP-12 expression is also regulated by ROS and NF-B (51, 52), the up-regulation of MMP-12 observed in Ig-Hepta Ϫ/Ϫ mice may be mediated via a similar mechanism.…”

Section: Discussionsupporting

confidence: 81%

“…They release various inflammatory mediators, including tumor necrosis factor (TNF)-␣, monocyte chemotactic protein (MCP)-1, and reactive oxygen species (ROS), which promote pulmonary inflammation (4 -6). It has been shown that ROS induce expression of macrophage matrix metalloproteinases (MMPs), including MMP-2, MMP-9, and MMP-12, through activation of the transcription factor nuclear factor-kappa B (NF-B) (7)(8)(9)(10)(11). MMPs are a family of Ca 2ϩ -activated Zn 2ϩ -dependent proteases that degrade the extracellular matrix, such as collagens, elastins, and gelatin (12).…”

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confidence: 99%

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Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation

Ariestanti

Ando

Hirose

et al. 2015

Journal of Biological Chemistry

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Background: Ig-Hepta knock-out mice exhibit emphysema-like symptoms, but their pathogenesis remains unclear. Results: In Ig-Hepta knock-out mice, alveolar macrophages are activated and release matrix metalloproteinases through reactive oxygen species-mediated nuclear factor-B activation. Conclusion: Ig-Hepta is likely to negatively regulate macrophage function and inflammation in the alveoli. Significance: These findings reveal a novel mechanism for maintaining lung homeostasis and immune regulation.

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Section: Discussionsupporting

confidence: 81%

mentioning

confidence: 99%

Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation

Ariestanti

Ando

Hirose

et al. 2015

Journal of Biological Chemistry

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“…For instance, it has been reported that EGCG inhibits the chymotrypsin-like activity of the proteasome, with IC 50 values in the range 86-194 nM, and subsequent accumulation of IjB-a [55]. This would result in inhibition of NF-jB activation and in downstream inhibition of NF-jB-regulated genes such as the matrixins [56,57].…”

Section: Discussionmentioning

confidence: 99%

Selective inhibition of ADAMTS‐1, ‐4 and ‐5 by catechin gallate esters

Vankemmelbeke

Jones

Fowles

et al. 2003

European Journal of Biochemistry

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Three mammalian ADAMTS enzymes, ADAMTS-1, -4 and -5, are known to cleave aggrecan at certain glutamyl bonds and are considered to be largely responsible for cartilage aggrecan catabolism observed during the development of arthritis. We have previously reported that certain catechins, polyphenolic compounds found in highest concentration in green tea (Camellia sinensis), are capable of inhibiting cartilage aggrecan breakdown in an in vitro model of cartilage degradation. We have now cloned and expressed recombinant human ADAMTS-1, -4 and -5 and report here that the catechin gallate esters found in green tea potently inhibit the aggrecan-degrading activity of these enzymes, with submicromolar IC 50 values. Moreover, the concentration needed for total inhibition of these members of the ADAMTS group is approximately two orders of magnitude lower than that which is needed to partially inhibit collagenase or ADAM-10 activity. Catechin gallate esters therefore provide selective inhibition of certain members of the ADAMTS group of enzymes and could constitute an important nutritional aid in the prevention of arthritis as well as being part of an effective therapy in the treatment of joint disease and other pathologies involving the action of these enzymes.Keywords: ADAMTS; enzyme inhibition; catechin; gallate; aggrecanase.Green tea, made from the leaves of Camellia sinensis, contains catechins, a group of polyphenolic compounds with antioxidant properties that have been at the centre of investigations into the potential medical benefits of consuming green tea. The most abundant catechin in green tea is (-)-epigallocatechin gallate (EGCG) with others such as (-)-epicatechin (EC), (-)-epigallocatechin (EGC) and (-)-epicatechin gallate (ECG) also present. Anti-inflammatory and anti-mitotic properties have been attributed to these compounds [1-3] and they have also been reported to inhibit certain matrixins such as the gelatinases [4][5][6]. The beneficial effects on a range of clinical conditions including cancer growth and metastasis [7][8][9][10][11], cardiovascular and liver diseases [12] may therefore be due to one or a combination of these properties.Aggrecan, a large aggregating proteoglycan, is together with type II collagen the major constituent of articular cartilage. Degradation of cartilage aggrecan has mainly been attributed to the action of glutamyl endopeptidases, termed ÔaggrecanasesÕ. Aggrecan degradation products resulting from aggrecanase action have been found in in vitro cultures of cartilage treated with proinflammatory cytokines as well as in synovial fluid of arthritis patients [13][14][15][16]. To date three mammalian ÔaggrecanasesÕ have been identified: a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-1, -4 and -5 [17][18][19]. The ADAMTS enzymes belong to a subgroup of metallopeptidases in Family M12 of Clan MA in the Merops database [20] and are related to the ADAMs and matrixins [21]. So far, at least 18 mammalian ADAMTS enzymes have been identified, most of which remain t...

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“…α-Lipoic acid (ALA, 1,2-dithiolane-3-pentanoic acid) is a naturally occurring antioxidant which inhibits TNF--induced NF-B activation and acts as a direct free-radical scavenger (Packer et al, 1995;Zhang and Frei, 2001). The promoter region of MMP-9 contains binding sites for NF-B (Sato and Seiki, 1993) and MMP-9 expression has been shown to be regulated by NF-B (Rajagopalan et al, 1996;Bond et al, 2001). Thus, we hypothesized that ALA α-Lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-κB transcriptional activity may inhibit MMP-9 expression by inhibiting NF-B activation.…”

Section: Introductionmentioning

confidence: 99%

α-Lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-κB transcriptional activity

Kim

Kim²,

Park³

et al. 2007

Exp Mol Med

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Abbreviations: ALA, α-lipoic acid; AP-1, activator protein-1; MMP-9, matrix metalloproteinase-9; VSMC, vascular smooth muscle cell AbstractThe migration of vascular smooth muscle cells (VSMCs) into the intima, an important step in injury-induced neointimal hyperplasia, requires the activation of nuclear factor-κB (NF-κB) and the consequent up-regulation of matrix metalloproteinase-9 (MMP-9). This study was undertaken to test for a possible effect of α-lipoic acid (ALA), a potent inhibitor of NF-κB, on MMP-9 expression. ALA inhibited high-glucose-and TNF-α-stimulated VSMC migrations in vitro. It also inhibited high-glucoseand TNF-α-induced increases in MMP-9 expression. The activity of MMP-9-promoter constructs with mutations in the NF-κB binding site was not inhibited by ALA, indicating an involvement of the NF-κB signaling pathway in the ALA-specific inhibition of MMP-9. These data suggest the possibility that ALA may be useful for the prevention of neointimal hyperplasia after angioplasty, by inhibiting the NF-κB/ MMP-9 pathway, especially with hyperglycemia.

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Inhibition of transcription factor NF-κB reduces matrix metalloproteinase-1, -3 and -9 production by vascular smooth muscle cells

Abstract: NF-kappaB is required for cytokine upregulation of MMP-1, -3 and -9 in VSMCs, which suggests that NF-kappaB inhibition may promote plaque stabilisation.

Cited by 332 publications

References 47 publications

Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation

Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation

Selective inhibition of ADAMTS‐1, ‐4 and ‐5 by catechin gallate esters

α-Lipoic acid inhibits matrix metalloproteinase-9 expression by inhibiting NF-κB transcriptional activity

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