Derepression of matrix metalloproteinase gene transcription and an emphysema‐like phenotype in transcription factor <i>Zbtb7c</i> knockout mouse lungs

Jeon, Bu‐Nam; Song, Jiwoon; Huh, Jin Won; Yang, W.J.; Hur, Man‐Wook

doi:10.1002/1873-3468.13501

Cited by 4 publications

(3 citation statements)

References 50 publications

(101 reference statements)

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“…Collagenase-3 levels were found to be upregulated in mice after long-term exposure to cigarette smoke and in patients with COPD [ 72 , 80 , 81 ]. MMP-13 expression in α1,6-fucosyltransferase-deficient mice and Zntb7 knockout mice was associated with the development of airspace enlargement and therefore with an emphysema-like phenotype [ 82 , 83 ]. In humans, MMP-13 has been shown to be involved in COPD exacerbations, as its levels remain elevated in smokers after viral infections [ 84 ].…”

Section: Mmps In Copdmentioning

confidence: 99%

“…More importantly, its expression is associated with small airway disease and the severity of emphysema [ 88 ]. Furthermore, MMP-10 in mice appeared to contribute to the development of cigarette-smoke-induced disease by directing macrophage–ECM macrophage remodeling [ 83 ]. Thus, MMP-10 appears to play an important role within the ECM assembly, suggesting that this proteinase is a relevant target for disease control.…”

Section: Mmps In Copdmentioning

confidence: 99%

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Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease

Christopoulou

Papakonstantinou

Stolz

2023

IJMS

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Matrix metalloproteinases (MMPs) are proteolytic enzymes that degrade proteins of the extracellular matrix and the basement membrane. Thus, these enzymes regulate airway remodeling, which is a major pathological feature of chronic obstructive pulmonary disease (COPD). Furthermore, proteolytic destruction in the lungs may lead to loss of elastin and the development of emphysema, which is associated with poor lung function in COPD patients. In this literature review, we describe and appraise evidence from the recent literature regarding the role of different MMPs in COPD, as well as how their activity is regulated by specific tissue inhibitors. Considering the importance of MMPs in COPD pathogenesis, we also discuss MMPs as potential targets for therapeutic intervention in COPD and present evidence from recent clinical trials in this regard.

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Section: Mmps In Copdmentioning

confidence: 99%

Section: Mmps In Copdmentioning

confidence: 99%

Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease

Christopoulou

Papakonstantinou

Stolz

2023

IJMS

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“…Inflammation is characterized by the infiltration of neutrophils, macrophages, and lymphocytes in the airways and lung parenchyma (Hogg et al, 2004;Brusselle et al, 2011;Faner et al, 2013). These inflammatory cells secrete a variety of proteinases, such as, neutrophils elastase (Hunninghake and Crystal, 1983;Ghosh et al, 2019), granulase (Ngan et al, 2009;Kim et al, 2013), matrix metalloproteinase (Ghosh et al, 2019;Jeon et al, 2019), and perforin (Morissette et al, 2007;Zhang et al, 2014), which break down the extracellular matrix, such as collagen and elastin, causing structural damage to the alveoli and small airways, thus leading to emphysema.…”

Section: Introductionmentioning

confidence: 99%

Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure

Wang

Liang

et al. 2021

Front. Mol. Biosci.

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Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease with high morbidity and mortality worldwide. So far, smoking is still its leading cause. The characteristics of COPD are emphysema and airway remodeling, as well as chronic inflammation, which were predominated by macrophages. Some studies have reported that macrophages were involved in emphysema and chronic inflammation, but whether there is a link between airway remodeling and macrophages remains unclear. In this study, we found that both acute and chronic cigarette smoke exposure led to an increase of macrophages in the lung and a decrease of ciliated cells in the airway epithelium of a mouse model. The results of in vitro experiments showed that the ciliary protein (β-tubulin-IV) levels of BEAS-2B cells could be inhibited when co-cultured with human macrophage line THP-1, and the inhibitory effect was augmented with the stimulation of cigarette smoke extract (CSE). Based on the results of transcriptome sequencing, we focused on the protein, bone morphogenetic protein-2 (BMP-2), secreted by the macrophage, which might mediate this inhibitory effect. Further studies confirmed that BMP-2 protein inhibited β-tubulin-IV protein levels of BEAS-2B cells under the stimulation of CSE. Coincidentally, this inhibitory effect could be nearly blocked by the BMP receptor inhibitor, LDN, or could be interfered with BMP-2 siRNA. This study suggests that activation and infiltration of macrophages in the lung induced by smoke exposure lead to a high expression of BMP-2, which in turn inhibits the ciliary protein levels of the bronchial epithelial cells, contributing to the remodeling of airway epithelium, and aggravates the development of COPD.

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The aberrant cross-talk of epithelium–macrophages via METTL3-regulated extracellular vesicle miR-93 in smoking-induced emphysema

Xia

Zhao

et al. 2021

Cell Biol Toxicol

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Derepression of matrix metalloproteinase gene transcription and an emphysema‐like phenotype in transcription factor Zbtb7c knockout mouse lungs

Cited by 4 publications

References 50 publications

Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease

Matrix Metalloproteinases in Chronic Obstructive Pulmonary Disease

Macrophages Inhibit Ciliary Protein Levels by Secreting BMP-2 Leading to Airway Epithelial Remodeling Under Cigarette Smoke Exposure

The aberrant cross-talk of epithelium–macrophages via METTL3-regulated extracellular vesicle miR-93 in smoking-induced emphysema

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