Expression Profile of Six RNA-Binding Proteins in Pulmonary Sarcoidosis

Navratilova, Zdenka; Novosadová, Eva; Hagemann-Jensen, Michael; Kullberg, Susanna; Kolek, Vı́tězslav; Grünewald, Johan; Petřek, Martin

doi:10.1371/journal.pone.0161669

Cited by 14 publications

(8 citation statements)

References 41 publications

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“… 51 Recently, decreased levels of AUF-1 mRNA were found in bronchoalveolar lavage cells and PBMC of patients with sarcoidosis, another chronic inflammatory lung disease. 52 The epithelial-specific loss of AUF-1 observed in COPD subjects in our study suggests that lower AUF-1 levels may become determinants of non-resolving inflammation, by altering the RNP complexes necessary for coordinate degradation of epithelial transcripts involved in the inflammatory response.…”

Section: Discussionmentioning

confidence: 60%

Differential expression of RNA-binding proteins in bronchial epithelium of stable COPD patients

Ricciardi¹,

Col²,

Casolari³

et al. 2018

COPD

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PurposeInflammatory gene expression is modulated by posttranscriptional regulation via RNA-binding proteins (RBPs), which regulate mRNA turnover and translation by binding to conserved mRNA sequences. Their role in COPD is only partially defined. This study evaluated RBPs tristetraprolin (TTP), human antigen R (HuR), and AU-rich element-binding factor 1 (AUF-1) expression using lung tissue from COPD patients and control subjects and probed their function in epithelial responses in vitro.Patients and methodsRBPs were detected by immunohistochemistry in bronchial and peripheral lung samples from mild-to-moderate stable COPD patients and age/smoking history-matched controls; RBPs and RBP-regulated genes were evaluated by Western blot, ELISA, protein array, and real-time PCR in human airway epithelial BEAS-2B cell line stimulated with hydrogen peroxide, cytokine combination (cytomix), cigarette smoke extract (CSE), and following siRNA-mediated silencing. Results were verified in a microarray database from bronchial brushings of COPD patients and controls. RBP transcripts were measured in peripheral blood mononuclear cell samples from additional stable COPD patients and controls.ResultsSpecific, primarily nuclear immunostaining for the RBPs was detected in structural and inflammatory cells in bronchial and lung tissues. Immunostaining for AUF-1, but not TTP or HuR, was significantly decreased in bronchial epithelium of COPD samples vs controls. In BEAS-2B cells, cytomix and CSE stimulation reproduced the RBP pattern while increasing expression of AUF-1-regulated genes, interleukin-6, CCL2, CXCL1, and CXCL8. Silencing expression of AUF-1 reproduced, but not enhanced, target upregulation induced by cytomix compared to controls. Analysis of bronchial brushing-derived transcriptomic confirmed the selective decrease of AUF-1 in COPD vs controls and revealed significant changes in AUF-1-regulated genes by genome ontology.ConclusionDownregulated AUF-1 may be pathogenic in stable COPD by altering posttranscriptional control of epithelial gene expression.

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Section: Discussionmentioning

confidence: 60%

Differential expression of RNA-binding proteins in bronchial epithelium of stable COPD patients

Ricciardi¹,

Col²,

Casolari³

et al. 2018

COPD

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“…Several studies have investigated the role of PTEN in the development and progression of pulmonary sarcoidosis. The protein and mRNA expression levels of PTEN in bronchoalveolar lavage (BAL) cells of sarcoid patients were reported similar to those in the BAL cells of normal patients [ 70 – 72 ]. However, activation of the PI3K/Akt pathway was observed [ 70 ].…”

Section: Pten In Chronic Lung Diseasesmentioning

confidence: 82%

PTEN: An Emerging Potential Target for Therapeutic Intervention in Respiratory Diseases

Cai

Yang

Jung

et al. 2022

Oxidative Medicine and Cellular Longevity

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Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a potent tumor suppressor that regulates several key cellular processes, including proliferation, survival, genomic integrity, migration, and invasion, via PI3K-dependent and independent mechanisms. A subtle decrease in PTEN levels or catalytic activity is implicated not only in cancer but also in a wide spectrum of other diseases, including various respiratory diseases. A systemic overview of the advances in the molecular and cellular mechanisms of PTEN involved in the initiation and progression of respiratory diseases may offer novel targets for the development of effective therapeutics for the treatment of respiratory diseases. In the present review, we highlight the novel findings emerging from current research on the role of PTEN expression and regulation in airway pathological conditions such as asthma/allergic airway inflammation, pulmonary hypertension (PAH), chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and other acute lung injuries (ALI). Moreover, we discuss the clinical implications of PTEN alteration and recently suggested therapeutic possibilities for restoration of PTEN expression and function in respiratory diseases.

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“…For instance, Li et al [17] found that the expression of RECK was significantly reduced in the lung tissues of COPD rats induced by chronic smoking. Navratilova et al [16] found that the expression of RECK in alveolar lavage fluid cells of COPD showed a downward trend. The low expression of RECK was also verified in in vitro cellular COPD model in our study.…”

Section: Discussionmentioning

confidence: 99%

Association between the Reduced Expression of RECK and Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease

Wang,

Su,

Liu

et al. 2024

Int Arch Allergy Immunol

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Introduction: Reversion-inducing cysteine-rich protein with Kazal motifs (RECK), a recently discovered inhibitor of matrix metalloproteinase (MMP). There is a large number of chronic obstructive pulmonary disease (COPD) patients worldwide; however, the role of RECK on COPD has not been studied. This study explored the expression of RECK in COPD patients and its effect on neutrophil function to provide a new scientific basis for the prevention and treatment of COPD. Method: Fifty patients with acute exacerbation of COPD and fifty healthy controls were enrolled in the study. RECK was detected in lung tissue, sputum, and plasma of subjects as well as in BEAS-2B cells stimulated with cigarette smoke extract (CSE) by immunohistochemistry, ELISA, and qRT-PCR. Meanwhile, lung function (FEV1%pred) and inflammatory cytokines (IL-6 and IL-8) were examined, and correlation analysis was performed with RECK expression. The effect of RECK on proliferation, apoptosis, migration, and inflammatory cytokines and its potential mechanism was further quantified by neutrophil stimulated with recombinant human RECK protein (rhRECK) combined with CSE using CCK8, flow cytometry, Transwell assay, qRT-PCR, ELISA, and Western analysis. Results: RECK was mainly expressed on airway epithelial cells in normal lung tissue and was significantly diminished in COPD patients. The levels of RECK in sputum and plasma were also significantly decreased in COPD patients. Pearson correlation analysis showed that RECK level in plasma was positively correlated with FEV1%pred (r = 0.458, p < 0.001) and negatively correlated with IL-6 and IL-8 (r = −0.386, −0.437; p = 0.006, 0.002) in COPD patients. The expression of RECK was decreased in BEAS-2B stimulated with CSE. The migration, inflammation, and MMP-9 expression of neutrophils were promoted by CSE, while inhibited by rhRECK. Conclusion: RECK is low expressed in COPD patients and negatively correlated with inflammation. It may inhibit the inflammation and migration of neutrophils by downregulating MMP-9.

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Expression Profile of Six RNA-Binding Proteins in Pulmonary Sarcoidosis

Cited by 14 publications

References 41 publications

Differential expression of RNA-binding proteins in bronchial epithelium of stable COPD patients

Differential expression of RNA-binding proteins in bronchial epithelium of stable COPD patients

PTEN: An Emerging Potential Target for Therapeutic Intervention in Respiratory Diseases

Association between the Reduced Expression of RECK and Neutrophilic Inflammation in Chronic Obstructive Pulmonary Disease

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