Montelukast suppresses epithelial to mesenchymal transition of bronchial epithelial cells induced by eosinophils

Hosoki, Koa; Kainuma, Keigo; Toda, Masaaki; Harada, Eijiro; Chelakkot-Govindalayathila, Ayshwarya-Lakshmi; Roeen, Ziaurahman; Nagao, Mizuho; D’Alessandro-Gabazza, Corina N.; Fujisawa, Takao; Gabazza, Esteban C.

doi:10.1016/j.bbrc.2014.05.033

Cited by 28 publications

(18 citation statements)

References 41 publications

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“…In addition, signal transduction cascades in HAECs are more likely to be dysregulated, affecting activation and differentiation of epithelial cells . In the present study, we demonstrated that eosinophils disrupted the expression of AJ and TJ in HAECs, which are comparable to the results of previous reports . In addition, LTE 4 was able to aggravate eosinophil‐induced epithelial disruption in AJ and TJ.…”

Section: Discussionsupporting

confidence: 90%

“…Montelukast was able to inhibit IL‐8 release from nasal epithelial cells in patients with asthma and allergic rhinitis . More importantly, convincing evidence showed that montelukast was able to reverse airway remodelling induced by eosinophils, which should be further elucidated by recovery of TJ and AJ proteins as shown in the present study. Taken together, dexamethasone and montelukast are involved in restoring epithelial activation and disintegrity induced by LTE 4 and eosinophils in AERD.…”

Section: Discussionsupporting

confidence: 70%

“…7,34 In the present study, we demonstrated that eosinophils disrupted the expression of AJ and TJ in HAECs, which are comparable to the results of previous reports. 26,35 In addition, Figure 3 could protect HAECs from the effects of LTE 4 and eosinophils, since claudin-1 is more relevant in TJ-strand formation 36 and permeability in cell layers. 37 IL-8 is documented to down-regulate the expression of TJ proteins 28 ; therefore, IL-8 decrease in shFLCN A549 cells incubated with LTE 4 and PBE may maintain the integrity of TJ and AJ proteins.…”

Section: Discussionmentioning

confidence: 99%

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Epithelial folliculin enhances airway inflammation in aspirin‐exacerbated respiratory disease

Trinh

Pham

Choi

et al. 2018

Clin Experimental Allergy

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

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Epithelial folliculin enhances airway inflammation in aspirin‐exacerbated respiratory disease

Trinh

Pham

Choi

et al. 2018

Clin Experimental Allergy

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“…Actions of CysLTs are mediated via GPCRs such as CysLT1 and CysLT2 [98]. LTD4 (100 nM) can suppress E-cadherin expression in cancer cells through enhanced translocation of -catenin to the nucleus while montelukast (0.1 mM) suppresses eosinophil-induced EMT in bronchial epithelial cells [99]. Recently, exosomes and cells from ascites in lung cancer patients can convert LTC4 to LTD4 to promote cancer cell migration and invasion via CysLT1 [100].…”

Section: Emt Inducers From Chronic Inflammatory Tumor Microenvironmentsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

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Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

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“…For example, montelukast treatment decreased eosinophils and other inflammatory cells in the lung biopsies as well as collagen and actin however not the elastic fibers in guinea pig model and it reduced expression of profibrotic molecules such as VEGF, TGF‐β as well as inflammatory cytokines such as IL‐4 and IL‐5 in mouse model of asthma . Moreover, montelukast treatment has been shown to decrease vimentin, collagen, tenascin, and laminin upon eosinophil stimulation; thus montelukast is thought to attenuate epithelial to mesenchymal transition associated with airway remodeling in asthma . However, montelukast increases intercellular adhesion molecule‐1 (ICAM‐1) expression, potentially leading to increased inflammatory cell migration to the lung, considering that chronic inflammation is the inducer of remodeling in asthma this latter finding contradicts the previous .…”

Section: Cysteinyl Leukotriene Receptor Antagonistsmentioning

confidence: 99%

Where does current and future pediatric asthma treatment stand? Remodeling and inflammation: Bird's eye view

Yılmaz

Yüksel

2016

Pediatr Pulmonol.

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Airway remodeling is the chronic outcome of inflammation in asthma and a point of intervention between pediatric and adult ages. Pediatric asthma has been of great interest in the efforts to find a valuable time to interrupt remodeling. Various experimental and clinical research have assessed the effect of current therapeutic modalities on airway remodeling in asthma and many new agents are being developed with promising results. The heterogeneity in the results of these studies may lie in the heterogeneity of pathogenesis leading to asthma and remodeling; underlying the need for individualized treatment of the unique pathogenetic characteristics of each child's asthma. The aim of this review is to summarize the evidence about the influence of current and future therapeutic modalities in the concept of inflammation and remodeling in pediatric asthma. Pediatr Pulmonol. 2016;51:1422-1429. © 2016 Wiley Periodicals, Inc.

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Montelukast suppresses epithelial to mesenchymal transition of bronchial epithelial cells induced by eosinophils

Cited by 28 publications

References 41 publications

Epithelial folliculin enhances airway inflammation in aspirin‐exacerbated respiratory disease

Epithelial folliculin enhances airway inflammation in aspirin‐exacerbated respiratory disease

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Where does current and future pediatric asthma treatment stand? Remodeling and inflammation: Bird's eye view

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