High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells

Chen, Yu Ching; Statt, Sarah; Wu, Reen; Chang, Hao Teng; Liao, Jiunn‐Wang; Wang, Chien Neng; Shyu, Woei Cherng; Lee, Chen Chen

doi:10.1038/srep18815

Cited by 58 publications

(51 citation statements)

References 59 publications

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“…Although previous studies have shown that e-cig-induced proinflammatory cytokine production, the role of HMGB1 in such exposures is not known (34,78). Our findings of increased HMGB1 release along with a decrease in E-cadherin suggest potential increase in inflammation and epithelial cell permeability, similar to situations with other injuries (17,48). Thus nicotine aerosol exposure via release of HMGB1 likely contributes toward increased epithelial and vascular permeability leading to pulmonary edema.…”

Section: Discussionsupporting

confidence: 53%

Acute pulmonary effects of aerosolized nicotine

Ahmad

Zafar

Mariappan

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Nicotine is a highly addictive principal component of both tobacco and electronic cigarette that is readily absorbed in blood. Nicotine-containing electronic cigarettes are promoted as a safe alternative to cigarette smoking. However, the isolated effects of inhaled nicotine are largely unknown. Here we report a novel rat model of aerosolized nicotine with a particle size (~1 μm) in the respirable diameter range. Acute nicotine inhalation caused increased pulmonary edema and lung injury as measured by enhanced bronchoalveolar lavage fluid protein, IgM, lung wet-to-dry weight ratio, and high-mobility group box 1 (HMGB1) protein and decreased lung E-cadherin protein. Immunohistochemical analysis revealed congested blood vessels and increased neutrophil infiltration. Lung myeloperoxidase mRNA and protein increased in the nicotine-exposed rats. Complete blood counts also showed an increase in neutrophils, white blood cells, eosinophils, and basophils. Arterial blood gas measurements showed an increase in lactate. Lungs of nicotine-inhaling animals revealed increased mRNA levels of IL-1A and CXCL1. There was also an increase in IL-1α protein. In in vitro air-liquid interface cultures of airway epithelial cells, there was a dose dependent increase in HMGB1 release with nicotine treatment. Air-liquid cultures exposed to nicotine also resulted in a dose-dependent loss of barrier as measured by transepithelial electrical resistance and a decrease in E-cadherin expression. Nicotine also caused a dose-dependent increase in epithelial cell death and an increase in caspase-3/7 activities. These results show that the nicotine content of electronic cigarettes may have adverse pulmonary and systemic effects.

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Section: Discussionsupporting

confidence: 53%

Acute pulmonary effects of aerosolized nicotine

Ahmad

Zafar

Mariappan

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…HMGB1 also functions as an inducer of EMT in human cancer cells (27)(28)(29)(30)(31). HMGB1 expression was much higher in bladder cancer cells than normal urethra epithelial cells and was associated with cell invasion (32,33).…”

Section: Introductionmentioning

confidence: 99%

LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR‑143/HMGB1 pathway

Luo

Chen

et al. 2017

Oncol Lett

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Abstract. The long non-coding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1) is an oncogenic lncRNA in bladder cancer, and its upregulation is associated with enhanced cell invasion. However, the underlying mechanism remains to be elucidated. The present study demonstrated that UCA1 was positively associated with cell invasion ability and promoted epithelial-mesenchymal transition (EMT) of bladder cancer cells by inducing high mobility group box 1 (HMGB1). Furthermore, bioinformatics and luciferase reporter assays demonstrated binding sites of the tumor suppressive miR-143 within UCA1 and the 3'untranslated region of HMGB1. UCA1 negatively regulated miR-143 expression in a dose-dependent manner in bladder cancer cells. In addition, UCA1 and HMGB1 were upregulated and miR-143 was downregulated in bladder cancer specimens. Overall, the data suggested that UCA1 may promote the invasion and EMT of bladder cancer cells by regulating the miR-143/HMGB1 pathway, which exhibits an important regulatory role in the pathology of bladder cancer.

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“…Interestingly, a recent study demonstrated increased expression of the SPARC family member, follistatin‐like protein 1 (FSTL1) in lung macrophages of patients with severe asthma, and further demonstrated that FSTL1 induces airway remodelling in mouse models of asthma (Miller et al, ). Moreover, it has recently been shown that the enigmatic protein high mobility group box 1 (HMGB1) induces SPARC expression in airway epithelial cells (Chen et al, ). This is of relevance, because HMGB1 is implicated in asthma and COPD (Sukkar et al, ) and has also been identified as a mediator of EMT and ECM synthesis in airway epithelial cells, thus suggesting a potential link between HMGB1 and SPARC signalling in chronic airways disease (Ojo et al, ; Chen et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, it has recently been shown that the enigmatic protein high mobility group box 1 (HMGB1) induces SPARC expression in airway epithelial cells (Chen et al, ). This is of relevance, because HMGB1 is implicated in asthma and COPD (Sukkar et al, ) and has also been identified as a mediator of EMT and ECM synthesis in airway epithelial cells, thus suggesting a potential link between HMGB1 and SPARC signalling in chronic airways disease (Ojo et al, ; Chen et al, ). Together with our discussion above, these studies provide further impetus for investigation of SPARC in asthma and COPD.…”

Section: Discussionmentioning

confidence: 99%

The SPARC protein: an overview of its role in lung cancer and pulmonary fibrosis and its potential role in chronic airways disease

Wong

Sukkar

2016

British J Pharmacology

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The SPARC (secreted protein acidic and rich in cysteine) protein is matricellular molecule regulating interactions between cells and their surrounding extracellular matrix (ECM). This protein thus governs fundamental cellular functions such as cell adhesion, proliferation and differentiation. SPARC also regulates the expression and activity of numerous growth factors and matrix metalloproteinases essential for ECM degradation and turnover. Studies in SPARC-null mice have revealed a critical role for SPARC in tissue development, injury and repair and in the regulation of the immune response. In the lung, SPARC drives pathological responses in non-small cell lung cancer and idiopathic pulmonary fibrosis by promoting microvascular remodelling and excessive deposition of ECM proteins. Remarkably, although chronic airway conditions such as asthma and chronic obstructive pulmonary disease (COPD) involve significant remodelling in both the airway and vascular compartments, the role of SPARC in these conditions has thus far been overlooked. In this review, we discuss the role of SPARC in lung cancer and pulmonary fibrosis, as well as potential mechanisms by which it may contribute to the disease process in asthma and COPD.Abbreviations COPD, chronic obstructive pulmonary disease; ECM, extracellular matrix; EMT, epithelial-mesenchymal transition; IPF, idiopathic pulmonary fibrosis; NSCLC, non-small cell lung cancer; PAI-1, plasminogen activator inhibitor-1; SPARC, secreted protein acidic and rich in cysteine

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High mobility group box 1-induced epithelial mesenchymal transition in human airway epithelial cells

Cited by 58 publications

References 59 publications

Acute pulmonary effects of aerosolized nicotine

Acute pulmonary effects of aerosolized nicotine

LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR‑143/HMGB1 pathway

The SPARC protein: an overview of its role in lung cancer and pulmonary fibrosis and its potential role in chronic airways disease

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