Regulation of metalloproteinase gene expression in normal and abnormal corneal repair

Fini, M E; Girard, M; Matsubara, Masahiko; Magner, JW; Mody, Monica; Rinehart, William B.; Strissel, Katherine J.

doi:10.1016/0014-4835(92)90460-a

Cited by 3 publications

(5 citation statements)

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“…However, we showed here that in rabbit dermal fibroblasts AP‐1 DNA binding is poorly regulated by cytokine and growth factor combinations implying that activation of AP‐1 binding alone is insufficient for synergistic upregulation of gelatinase‐B. This suggests the interaction with additional factors, of which NF‐κB is an attractive possibility because a functional NF‐κB binding element exists in the gelatinase‐B promoter in a region that cooperates with the proximal AP‐1 element [7, 9]. Moreover, stable expression of a dominant negative NF‐κB/p65 mutant partially inhibited IL‐1β induced MMP‐9 expression in mesangial cells [10].…”

Section: Discussionmentioning

confidence: 85%

“…TNF‐α and IL‐1α activate receptor tyrosine kinase independent pathways, leading to the rapid activation of NF‐κB. From previous studies, the AP‐1 transcription factor is known to be essential for MMP‐9 expression in fibroblasts [7, 9]. However, we showed here that in rabbit dermal fibroblasts AP‐1 DNA binding is poorly regulated by cytokine and growth factor combinations implying that activation of AP‐1 binding alone is insufficient for synergistic upregulation of gelatinase‐B.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have highlighted the absolute requirement for a conserved proximal AP‐1 binding site in the induction of MMP‐9 [7–10]. A distal stimulatory region encompassing an NF‐κB element and an additional AP‐1 binding site [7, 9]has also been identified although it is uncertain whether this is also essential or merely cooperates with the proximal AP‐1 site. We used electromobility shift assays and adenoviral mediated overexpression of IκBα, the endogenous inhibitor of NF‐κB, to determine the importance of NF‐κB in upregulation of MMP‐9.…”

Section: Introductionmentioning

confidence: 99%

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Synergistic upregulation of metalloproteinase‐9 by growth factors and inflammatory cytokines: an absolute requirement for transcription factor NF‐κB

et al. 1998

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Matrix metalloproteinase (MMPs) enzymes are implicated in matrix remodelling during proliferative inflammatory processes including wound healing. We report here synergistic upregulation of MMP-9 protein and mRNA by platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in combination with interleukin-1K K (IL-1K K) or tumour necrosis factor-K K (TNF-K K) in primary rabbit and human dermal fibroblasts. The synergistic interaction between growth factors and cytokines implies that basement membrane remodelling is maximal physiologically when both are present together. The signalling pathways mediating this synergistic regulation are not understood, although analysis of the MMP-9 promoter has identified an essential proximal AP-1 element and an upstream nuclear factor kappa-B (NF-U UB) site. Using electromobility shift assays, binding to the AP-1 site was only slightly increased by growth factors and cytokines. NF-U UB binding was rapidly induced by IL-1K K or TNF-K K but was neither induced nor potentiated by bFGF or PDGF. Neither AP-1 nor NF-U UB was therefore sufficient on its own for synergistic regulation. Using a recently developed adenovirus that overexpresses the inhibitory subunit, IU UBK K, we demonstrated an absolute requirement for NF-U UB in upregulation of MMP-9. Activation of NF-U UB binding by inflammatory cytokines was therefore necessary but not sufficient for synergistic upregulation of MMP-9.z 1998 Federation of European Biochemical Societies.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Synergistic upregulation of metalloproteinase‐9 by growth factors and inflammatory cytokines: an absolute requirement for transcription factor NF‐κB

et al. 1998

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“…Transcription of the MMP9 gene was strongly induced when corneal cells are exposed to bacteria [34, 35]. MMP9 is involved in remodeling of the corneal basement membrane and regulates corneal healing, but has also been linked with corneal perforation [36, 37]. Tetracyclines inhibit MMP9 activity, and that is one reason that tetracyclines have been given systemically to patients with corneal ulcers or perforations [38].…”

Section: Discussionmentioning

confidence: 99%

Predatory Bacteria can ReducePseudomonas aeruginosaInduced Corneal Perforation and Proliferation in a Rabbit Keratitis Model

Romanowski

Stella

Brazile

et al. 2023

Preprint

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Purpose: Pseudomonas aeruginosa keratitis is a severe ocular infection that can lead to perforation of the cornea. In this study we evaluated the role of bacterial quorum sensing in generating corneal perforation and bacterial proliferation and tested whether co-injection of the predatory bacteria Bdellovibrio bacteriovorus could alter the clinical outcome. P. aeruginosa with lasR mutations were observed among keratitis isolates from a study collecting samples from India, so an isogenic lasR mutant strain of P. aeruginosa was included. Methods: Rabbit corneas were intracorneally infected with P. aeruginosa strain PA14 or an isogenic ΔlasR mutant and co-injected with PBS or B. bacteriovorus. After 24 h, eyes were evaluated for clinical signs of infection. Samples were analyzed by scanning electron microscopy, optical coherence tomography, sectioned for histology, and corneas were homogenized for CFU enumeration and for inflammatory cytokines. Results: We observed that 54% of corneas infected by wild-type PA14 presented with a corneal perforation (n=24), whereas only 4% of PA14 infected corneas that were co-infected with B. bacteriovorus perforate (n=25). Wild-type P. aeruginosa proliferation was reduced 7-fold in the predatory bacteria treated eyes. The ΔlasR mutant was less able to proliferate compared to the wild-type, but was largely unaffected by B. bacteriovorus. Conclusion: These studies indicate a role for bacterial quorum sensing in the ability of P. aeruginosa to proliferate and cause perforation of the rabbit cornea. Additionally, this study suggests that predatory bacteria can reduce the virulence of P. aeruginosa in an ocular prophylaxis model.

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“…MMP-9 has also been cloned in many other mammalians such as rats [59], mice [60], cows [61] and rabbits [62], and a high homology between human and other species has been confirmed. MMP-9 is not ordinarily generated by pulmonary resident cells in normal condition, but once inflammation such as asthma exacerbation has been switched on a wide range of inflammatory and structural cells can produce MMP-9.…”

Section: The Cellular Source Of Mmp-9 In Asthmamentioning

confidence: 94%

Matrix Metalloproteinase-9 and Airway Remodeling in Asthma

Ohbayashi¹,

Shimokata

2005

CDTIA

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Airway remodeling is a major change responsible for irreversible asthmatic airflow restriction. The Th-2 cytokines-dominant eosinophilic inflammatory mechanism cannot fully explain the progressive subepithelial fibrosis and structural changes in the extracellular matrix (ECM). Matrix metalloproteinases (MMPs) are the key enzymes responsible for ECM degradation. MMPs are normally produced and secreted under the tight regulation of, at least, 3 different levels: the gene transcriptional level, the activation of the latent form of enzyme, and the inactivation by specific endogenous inhibitors. In asthmatic condition, as shown by the large amount of accumulated evidence in this review, MMP-9 is the most relevant among the 23 kinds of human MMPs at present detected. Although the mechanism is still under investigation and not accurately known, the imbalance between MMP-9 and tissue inhibitor of metalloproteinase-1 is considered a major theory to explain the progression of asthmatic airway remodeling. Various inflammatory cytokines including TGF beta and growth factors play a pivotal role in MMP-9 production and secretion. This review mainly focuses upon the pivotal role of MMP-9 in airway remodeling, and also upon major cellular source of MMP-9 in asthma such as eosinophils, neutrophils, epithelial cells and alveolar macrophages. This review also refers to the partial contribution of nitric oxide to MMP-9 in asthma.

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Regulation of metalloproteinase gene expression in normal and abnormal corneal repair

Cited by 3 publications

References 0 publications

Synergistic upregulation of metalloproteinase‐9 by growth factors and inflammatory cytokines: an absolute requirement for transcription factor NF‐κB

Synergistic upregulation of metalloproteinase‐9 by growth factors and inflammatory cytokines: an absolute requirement for transcription factor NF‐κB

Predatory Bacteria can ReducePseudomonas aeruginosaInduced Corneal Perforation and Proliferation in a Rabbit Keratitis Model

Matrix Metalloproteinase-9 and Airway Remodeling in Asthma

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