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PubMed Journal Database | American journal of respiratory cell and molecular biology RSS

04:43 EDT 19th October 2018 | BioPortfolio

The US National Library of Medicine and National Institutes of Health manage PubMed.gov which comprises of more than 21 million records, papers, reports for biomedical literature, including MEDLINE, life science and medical journals, articles, reviews, reports and  books.  BioPortfolio aims to publish relevant information on published papers, clinical trials and news associated with users selected topics.

For example view all recent relevant publications on Epigenetics and associated publications and clincial trials.

Showing PubMed Articles 1–25 of 388 from American journal of respiratory cell and molecular biology

Environment, Epigenetics, and Differential Responses to Beryllium Exposure: Are We There Yet?

Fibronectin on the Surface of Extracellular Vesicles Mediates Fibroblast Invasion.

Extracellular vesicles (EVs) are endosome and plasma membrane-derived nanosized vesicles that participate in intercellular signaling. Although EV cargo may signal via multiple mechanisms, how signaling components on the surface of EVs mediate cellular signaling is less well understood. In this study, we show that fibroblast-derived EVs carry fibronectin on the vesicular surface, as evidenced by mass spectrometry-based proteomics (sequential windowed acquisition of all theoretical peptides; SWATH) and flow c...

HIV-Nef Protein Persists in the Lungs of Aviremic HIV Patients and Induces Endothelial Cell Death.

It remains a mystery why HIV-associated end-organ pathologies persist in the era of combined antiretroviral therapy (ART). One possible mechanism is the continued production of HIV encoded proteins in latently HIV-infected T cells and macrophages. The pro-apoptotic protein HIV-Nef persists in the blood of ART treated patients within extracellular vesicles (EV) and PBMC. Here we demonstrate that HIV-Nef is present in cells and extracellular vesicles (EV) isolated from bronchoalveolar lavage (BAL) of patients...

Myeloid TBK1 Signaling Contributes to the Immune Response to Influenza.

Macrophages provide key elements of the host response to influenza A virus (IAV) infection, including expression of type I interferon (IFN) and inflammatory cytokines and chemokines. TANK-binding kinase 1 (TBK1) contributes to IFN expression and anti-viral responses in some cell types, but its role in the innate response to IAV in vivo is unknown. We hypothesized that macrophage TBK1 contributes to both IFN and non-IFN components of host defense and IAV pathology. We generated myeloid-conditional TBK1 knock...

Special Delivery: A New Package for an Old Anti-Fibrotic Mediator.

Macrophage Polarization in Sarcoidosis: An Unexpected Accomplice?

Dusting Off Interleukin-9 as a New Therapeutic Target for Pulmonary Fibrosis.

TREM-1 Attenuates RIPK3 Mediated Necroptosis in Hyperoxia Induced Lung Injury in Neonatal Mice.

Hyperoxia-induced injury to the developing lung, impaired alveolarization and dysregulated vascularization are critical factors in the pathogenesis of bronchopulmonary dysplasia (BPD); however, mechanisms for hyperoxia-induced development of BPD are not fully known. Here we show that the triggering receptor expressed on myeloid cells 1 (TREM-1) is upregulated in hyperoxia-exposed neonatal mice lungs as well as in tracheal aspirates (TA) and lungs of human neonates with respiratory distress syndrome (RDS) an...

S100A8 Protects Human Primary Alveolar Type II Cells Against Injury and Emphysema.

Pulmonary emphysema is characterized by alveolar wall destruction and cigarette smoking is the main factor of this disease development. S100A8 is a member of the S100 protein family with oxidative stress-related and anti-inflammatory role. The mechanisms of human alveolar type II (ATII) cell injury leading to emphysema pathophysiology are not completely understood. We wanted to determine whether S100A8 can protect ATII cells against injury induced by cigarette smoke and this disease development. We used fre...

Nitric Oxide Synthase 2 Induction Promotes Right Ventricular Fibrosis.

The ability of the right ventricle (RV) to compensate pressure overload is determining survival in pulmonary arterial hypertension (PAH). Nitric oxide (NO) reduces the RV afterload through pulmonary vasodilation, but excessive NO amounts cause oxidative stress. Oxidative stress drives remodeling of pulmonary arteries and the RV. Here, we hypothesized that NO synthase 2 (NOS2) induction leads to excessive NO amounts that contribute to oxidative stress and impairs RV adaption to PAH. We utilized a surgical pu...

P-311 in Scar Wars: Myofibroblasts Lost without TGFβ Translation.

Alveolar Epithelial Cells Burn Fat to Survive Acute Lung Injury.

Activated Human Lung Fibroblasts Produce Extracellular Vesicles with Anti-Fibrotic Prostaglandins.

The differentiation of interstitial lung fibroblasts into contractile myofibroblasts that proliferate and secrete excessive extracellular matrix is critical in the pathogenesis of pulmonary fibrosis. Certain lipid signaling molecules such as prostaglandins can inhibit myofibroblast differentiation. However, the sources and delivery mechanisms of endogenous prostaglandins are undefined. Activated primary human lung fibroblasts (HLFs) produce prostaglandins such as PGE2. We report that activation of primary H...

Interleukin-9 Blockade Suppresses Silica-induced Lung Inflammation and Fibrosis in Mice.

Recapitulative animal models of idiopathic pulmonary fibrosis (IPF) and related diseases are lacking, which inhibits our ability to fully clarify the pathogenesis of these diseases. Although lung fibrosis in mouse models is often induced by bleomycin, silica-induced lung fibrosis is more sustainable and more progressive. Therefore, in this study, we sought to elucidate the mediator(s) responsible for the pathogenesis of lung fibrosis through the use of a mouse model of silica-induced lung fibrosis. With a s...

Sex Differences in Pulmonary Responses to Ozone in Mice: Role of the Microbiome.

We have previously reported that the mouse gut microbiome contributes to pulmonary responses to ozone, a common asthma trigger, and that short chain fatty acids, end products of bacterial fermentation, likely contribute to this role of the microbiome. A growing body of evidence indicates sex-related differences in gut microbiota and that these differences can have important functional consequences. The purpose of this study was to determine whether there were sex-related differences in the impact of the gut...

Recommended Reading from the National University of Ireland Galway Regenerative Medicine Institute (REMEDI) Lung Biology Group Fellows.

A Non-Hospitable Host: Targeting Cellular Factors as an Antiviral Strategy for Respiratory Viruses.

P311 Promotes Lung Fibrosis via Stimulation of TGF-β1, 2 and 3 Translation.

Interstitial lung fibrosis, a frequently idiopathic and fatal disease, has been linked to the increased expression of profibrotic TGF-βs. P311 is an RNA-binding protein, which stimulates TGF-β1, 2 and 3 translation in several cell types through its interaction with the eukaryotic translation initiation factor 3b. Here we report that P311 is switched on in the lungs of Idiopathic pulmonary fibrosis (IPF) patients and in the mouse model of bleomycin (BLM)-induced pulmonary fibrosis. To assess the in vivo ro...

Induced Pluripotent Stem Cells for Primary Ciliary Dyskinesia Modeling and Personalized Medicine.

Primary ciliary dyskinesia (PCD) is a rare and heterogeneous genetic disorder that affects the structure and function of motile cilia. In the airway epithelium, impaired ciliary motion results in reduced or absent mucociliary clearance that leads to the appearance of chronic airway infection, sinusitis and bronchiectasis. Currently, there is no effective treatment for PCD, and research is limited by the lack of convenient models to study this disease and investigate innovative therapies. Furthermore, the hi...

Intercellular Communication between Airway Epithelial Cells is Mediated by Exosome-Like Vesicles.

Airway epithelium structure/function can be altered by local inflammatory/immune signals, and this process is called epithelial remodeling. The mechanism by which this innate response is regulated, which causes mucin/mucus overproduction, is largely unknown. Exosomes are nano-vesicles that can be secreted and internalized by cells to transport cellular cargo, such as proteins, lipids, and miRNA. The objective of this study was to understand the role exosomes play in airway remodeling through cell-cell commu...

Relation Between Respiratory Mechanics, Inflammation, and Survival in Experimental Mechanical Ventilation.

Low tidal volume ventilation might protect healthy lungs from volutrauma but lead to inflammation from other mechanisms, namely alveolar derecruitment and the ensuing alveolar collapse and reexpansion.

Could Immunotherapy Sink its Teeth into LAM?

BETting on Novel Treatments for Asthma: Bromodomain 4 Inhibitors.

Efficacy of Novel Highly Specific Bromodomain-Containing Protein 4 Inhibitors in Innate Inflammation-Driven Airway Remodeling.

NFκB/RelA triggers innate inflammation by binding to Bromodomain-Containing Protein 4 (BRD4), an atypical histone acetyltransferase (HAT). Although RelA·BRD4 HAT mediates acute neutrophilic inflammation, its role in chronic and functional airway remodeling is not known. We observed that BRD4 is required for TLR3 mediated mesenchymal transition, a cell-state change that is characteristic of remodeling. We therefore tested novel highly selective BRD4 inhibitors, ZL0420 and -0454, on chronic airway remodelin...

Influenza in Smokers - More than Just a Cause of Symptom Exacerbations?


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