MicroRNA-146a modulates human bronchial epithelial cell survival in response to the cytokine-induced apoptosis

Liu, Xiangde; Nelson, Amy; Wang, Xingqi; Kanaji, Nobuhiro; Kim, Miok; Satô, Tadashi; Nakanishi, Masayoshi; Li, Ying Ji; Sun, Jianhong; Michalski, Joel; Patil, Amol; Basma, Hesham; Rennard, Stephen I.

doi:10.1016/j.bbrc.2009.01.066

Cited by 59 publications

(42 citation statements)

References 38 publications

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“…miRNAs are approximately 22-nucleotide RNAs that promote mRNA degradation (34) or inhibit translation (35), by binding with at least partial complementarity to the 39 untranslated region of target mRNAs. miRNAs have been implicated in the regulation of fundamental biological processes in epithelial cells such as cell proliferation, differentiation, and apoptosis (36)(37)(38). One focus of our ongoing work is to study whether these miRNAs regulate asthma-relevant biological functions of these epithelial cells.…”

Section: Airway Epithelial Micrornas As Endotypic Markersmentioning

confidence: 99%

Subtypes of Asthma Defined by Epithelial Cell Expression of Messenger RNA and MicroRNA

Woodruff

2013

Annals ATS

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Human asthma can be subcategorized in several ways, but one powerful approach is to subtype asthma on the basis of underlying cellular and molecular mechanisms. Groups of patients with a disease that share a common underlying biology are termed an "endotype." Endotypes of asthma have been studied at both the cellular level (by cytological examination of induced sputum) and, increasingly, at the molecular level. Genome-wide analyses of mRNA expression within the lung have been useful in the identification of molecular endotypes of asthma and point to protein biomarkers of those endotypes that can be measured in the blood. More recently, studies of microRNA expression in airway epithelial cells in asthma have identified additional candidate biomarkers of asthma endotypes. One potentially valuable property of microRNAs is that they can also be measured in extracellular fluids and therefore have the potential to serve directly as noninvasively measured biomarkers.

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Section: Airway Epithelial Micrornas As Endotypic Markersmentioning

confidence: 99%

Subtypes of Asthma Defined by Epithelial Cell Expression of Messenger RNA and MicroRNA

Woodruff

2013

Annals ATS

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“…miR-146a has been previously reported as a key factor for innate immune system in balance toward cell survival (18). In addition, miR-146a appeared to modulate epithelial cell survival through upregulation of Bcl-xl and STAT3 (15) and is also associated with the risk for hepatocellular carcinoma (32). However, a functional role of miR-146a in survival and cytoprotection of stem cell is unknown.…”

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confidence: 92%

Diazoxide potentiates mesenchymal stem cell survival via NF-κB-dependent miR-146a expression by targeting Fas

Suzuki

Kim

Ashraf

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…Whether miRNAs help regulate changes in epithelial gene expression, cell differentiation, and function in asthma is uncertain. However, several miRNAs have been implicated in epithelial cell proliferation, differentiation, and apoptosis (15)(16)(17). Furthermore, miR-449, a member of the miR-34/449 family, was recently identified as a critical regulator of differentiation of nasal epithelial cells to ciliated cells by directly repressing transcript levels of NOTCH1 and its ligand DLL1 (18).…”

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confidence: 99%

Airway Epithelial miRNA Expression Is Altered in Asthma

Solberg

Ostrin

Love

et al. 2012

Am J Respir Crit Care Med

222

261

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Rationale: Changes in airway epithelial cell differentiation, driven in part by IL-13, are important in asthma. Micro-RNAs (miRNAs) regulate cell differentiation in many systems and could contribute to epithelial abnormalities in asthma. Objectives: To determine whether airway epithelial miRNA expression is altered in asthma and identify IL-13-regulated miRNAs. Methods:We used miRNA microarrays to analyze bronchial epithelial brushings from 16 steroid-naive subjects with asthma before and after inhaled corticosteroids, 19 steroid-using subjects with asthma, and 12 healthy control subjects, and the effects of IL-13 and corticosteroids on cultured bronchial epithelial cells. We used quantitative polymerase chain reaction to confirm selected microarray results. Measurements and Main Results: Most (12 of 16) steroid-naive subjects with asthma had a markedly abnormal pattern of bronchial epithelial miRNA expression by microarray analysis. Compared with control subjects, 217 miRNAs were differentially expressed in steroid-naive subjects with asthma and 200 in steroid-using subjects with asthma (false discovery rate , 0.05). Treatment with inhaled corticosteroids had modest effects on miRNA expression in steroid-naive asthma, inducing a statistically significant (false discovery rate , 0.05) change for only nine miRNAs. qPCR analysis confirmed differential expression of 22 miRNAs that were highly differentially expressed by microarrays. IL-13 stimulation recapitulated changes in many differentially expressed miRNAs, including four members of the miR-34/ 449 family, and these changes in miR-34/449 family members were resistant to corticosteroids. Conclusions: Dramatic alterations of airway epithelial cell miRNA levels are a common feature of asthma. These alterations are only modestly corrected by inhaled corticosteroids. IL-13 effects may account for some of these alterations, including repression of miR-34/449 family members that have established roles in airway epithelial cell differentiation. Clinical trial registered with www.clinicaltrials.gov (NCT 00595153).Keywords: miRNA; asthma; airway epithelium Asthma is an inflammatory condition of the lung characterized by episodic airway obstruction and remodeling of airway tissues (1). The airway epithelium is increasingly recognized as an important participant in asthma pathophysiology (2, 3). Airway epithelial cells produce mucus, which is a major contributor to airway obstruction in fatal asthma (4), and even patients with stable mild and moderate asthma have increased epithelial mucin stores (5). Previous human, animal model, and cell culture studies demonstrate that the Th2 cytokine IL-13 is a critical inducer of airway epithelial abnormalities in asthma (6-8). IL-13 stimulation of epithelial cells leads to an increase in the number of mucous cells (mucous metaplasia) and a decrease in the number of ciliated cells (9). IL-13 stimulation of airway epithelial cells activates signal transduction and transcription factor 6, leading to changes in expression of mRNAs that...

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MicroRNA-146a modulates human bronchial epithelial cell survival in response to the cytokine-induced apoptosis

Cited by 59 publications

References 38 publications

Subtypes of Asthma Defined by Epithelial Cell Expression of Messenger RNA and MicroRNA

Subtypes of Asthma Defined by Epithelial Cell Expression of Messenger RNA and MicroRNA

Diazoxide potentiates mesenchymal stem cell survival via NF-κB-dependent miR-146a expression by targeting Fas

Airway Epithelial miRNA Expression Is Altered in Asthma

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