Early Increased Levels of Matrix Metalloproteinase-9 in Neonates Recovering from Respiratory Distress Syndrome

Dik, Willem A.; Kaam, A.H.L.C. van; Dekker, Tamara; Naber, Brigitta A.E.; Janssen, Daphne J.; Kroon, Abraham A.; Zimmermann, Luc J. I.; Versnel, Marjan A.; Lutter, René

doi:10.1159/000088193

Cited by 28 publications

(32 citation statements)

References 38 publications

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“…Increased production of MMP-9 from infiltrating immune cells or from the respiratory epithelium occurs in inflammatory lung diseases, and abnormal expression and activation of MMP-9 tend to accompany tissue injury and airway remodeling (Okamoto et al, 2002;Dik et al, 2005). Cataldo et al showed that deletion of the MMP-9 gene reduces peribronchial inflammation, airway lymphocyte accumulation, airway IL-13 production and the development of bronchial hyperresponsiveness (2002).…”

Section: Discussionmentioning

confidence: 99%

PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

Shin

Yoon²,

Choe³

et al. 2007

Exp Mol Med

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Expression of matrix metalloproteinase-9 (MMP-9) is associated with airway remodeling and tissue injury in asthma. However, little is known about how MMP-9 is up-regulated in airway epithelial cells. In this study, we show that phorbol myristate acetate (PMA) induces MMP-9 expression via a protein kinase Cα (PKCα)-dependent signaling cascade in BEAS-2B human lung epithelial cells. Pretreatment with either GF109203X, a general PKC inhibitor, or Gö6976, a PKCα/β isozyme inhibitor, inhibited PMA-induced activation of the MMP-9 promoter, as did transient transfection with PKCα antisense oligonuclotides. PMA activated NF-κB by phosphorylating IκB in these cells and this was also inhibited by GF109203X and Gö6976, suggesting that PKCα acts as an upstream regulator of NF-κB in PMA-induced MMP-9 induction. Our results indicate that a "PKCα-NF-κB"-dependent cascade is involved in the signaling leading to PMA-induced MMP-9 expression in the lung epithelium.

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Section: Discussionmentioning

confidence: 99%

PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

Shin

Yoon²,

Choe³

et al. 2007

Exp Mol Med

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“…Indeed, for severely premature neonates, BPD/CLD shows progression towards impairment of alveolar septation from enhanced proteolysis of extracellular matrix components (30,77), coinciding with increased appearance of a number of enzymes such as neutrophil elastase and matrix metalloproteinase (MMP)-8 (20,77,79). Recent data suggest that disruption of angiogeneis (36) prevents alveolarization and development of other distal lung air space architecture (81,82), which is a major hallmark of BPD.…”

mentioning

confidence: 99%

Effect of covalent antithrombin-heparin complex on developmental mechanisms in the lung

Parmar

Berry²,

Post³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The NGAL functions mainly depend on its binding activity, directed against various molecules, such as N-formylated tripeptides, fatty acids, leukotriene B4 and platelet activating factor (3) as well as plasma matrix metallo-protein MMP-9 (4). In particular, when bound to MMP-9, NGAL may modulate various inflammatory mechanisms, including acute phase proteins and the vascular repair process (5)(6)(7)(8).…”

mentioning

confidence: 99%

“…In fact, indometacin, a drug used in cases ofnewborn PDA, has been reported to decrease MMP-9 synthesis and release (10)(11) and also to reduce IL-l-beta (6)(7)(8) up-regulation of NGAL, although in a different field and in a rat model (7,12). Dexamethasone or retinoic acid treatment are able to increase NGAL synthesis as well as oxygenation (13), vascular injury and oxidative stress (14).…”

mentioning

confidence: 99%

“…Dexamethasone or retinoic acid treatment are able to increase NGAL synthesis as well as oxygenation (13), vascular injury and oxidative stress (14). Increased NGAL levels have recently been .found at the 2 nd and 4 th day of life in BALF of premature infants not developing bronchopulmonary disease (BPD) (8), while subsequent increases were observed on the T" and l O" day in BPD infants. Further observations have been reported by Sveger T et al (16) on sera, showing no association with BPD.…”

mentioning

confidence: 99%

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Epithelial Lining Fluid Neutrophil-Gelatinase-Associated Lipocalin Levels in Premature Newborns with Bronchopulmonary Dysplasia and Patency of Ductus Arteriosus

Capoluongo

Vento

Lulli

et al. 2008

Int J Immunopathol Pharmacol

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Patency of the ductus arteriosus (PDA) and bronchopulmonary dysplasia (BPD) development represent severe affections for premature newborns, therefore the research of early markers for these two conditions is really important. The aim of this study is to analyze epithelial lining fluid (ELF) Neutrophil-gelatinase-associated lipocalin (NGAL) levels for prediction of lung injury or possible involvement ofthis molecule in PDA. Only scarce and contrasting results have previously been published in this field. In contrast, this molecule, included in a large macromolecular complex together with matrix metalloproteinase-9 (MMP-9), is considered an acceptable marker of infectious/inflammatory processes, cancer monitoring and induction of apoptotic pathway. NGAL was detected in 28 pre-term newborns by means of a commercially available kit in bronchoalveolar lavage fluid (BALF). The results have been corrected to ELF levels, by the urea method, to eliminate bias due to BALF collection. ELF NGAL levels were found significantly increased both in infants developing BPD or in those affected by PDA. By means of multivariate logistic regression analysis the significances were confirmed after adjusting for possible interfering variables such as gestational age and concomitant presence of both PDA and BPD. Our results stress the involvement of NGAL in the mechanisms leading to BPD and also suggest a possible association with PDA, which is often linked to prematurity and BPD development, probably due to the involvement of inflammatory and angiogenetic processes in both pathologies.Neutrophil-gelatinase-associated lipocalin (NGAL) is a 25-kDa protein associated with neutrophil ge1atinase, a molecular complex of 220-kDa, (namely matrix metallo-protein-9, MMP-9) including a homodimer of the gelatinase component (92-kDa) and the NGAL protein (l). NGAL is present in monocyte/macrophage cell lineage, in hepatocyte, epithelial and immune cells. It has been shown to increase in inflammatory and neoplastic diseases and has been proposed as a kidney injury marker (2). The NGAL functions mainly depend on its binding activity, directed against various molecules, such as N-formylated tripeptides, fatty acids, leukotriene B4 and platelet activating factor (3) as well as plasma matrix metallo-protein MMP-9 (4). In particular, when bound to MMP-9, NGAL may modulate

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Early Increased Levels of Matrix Metalloproteinase-9 in Neonates Recovering from Respiratory Distress Syndrome

Cited by 28 publications

References 38 publications

PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

PMA-induced up-regulation of MMP-9 is regulated by a PKCα-NF-κB cascade in human lung epithelial cells

Effect of covalent antithrombin-heparin complex on developmental mechanisms in the lung

Epithelial Lining Fluid Neutrophil-Gelatinase-Associated Lipocalin Levels in Premature Newborns with Bronchopulmonary Dysplasia and Patency of Ductus Arteriosus

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