Advertisement

Topics

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

14:34 EST 19th January 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 351 from American journal of respiratory cell and molecular biology

R-spondin 2 is Upregulated in Idiopathic Pulmonary Fibrosis and Affects Fibroblasts Behavior.

Idiopathic pulmonary fibrosis (IPF) is characterized by the expansion of the myofibroblasts population, excessive extracellular matrix accumulation, and destruction of the lung parenchyma. The R-spondins family (RSPO) comprises a group of proteins essential for development. From them, RSPO2 is expressed primarily in the lungs and its mutations cause severe defects in the respiratory tract. Interestingly, RSPO2 participates in the canonical WNT pathway, a critical route in the pathogenesis of IPF. Thus, the ...

Novel Mechanism for Nicotinamide Phosphoribosyltransferase Inhibition of TNF-α-Mediated Apoptosis in Human Lung Endothelial Cells.

Nicotinamide phosphoribosyltransferase (NAMPT) exists as both intracellular (iNAMPT) and extracellular (eNAMPT) proteins. eNAMPT is secreted into the blood and functions as a cytokine/enzyme (cytozyme) that activates NFκB signaling via ligation of the TLR4 receptor, further serving as a biomarker for inflammatory lung disorders such as the acute respiratory distress syndrome (ARDS). In contrast, iNAMPT is involved in nicotinamide mononucleotide (NMN) synthesis and has been implicated in the regulation of c...

Is Asthma Paying the Toll?

January Highlights/Papers by Junior Investigators/NIH News.

Monocyte-derived Alveolar Macrophages: The Dark Side of Lung Repair?

High-Mobility Group Box 1 Upregulates MUC5AC and MUC5B Expression in Primary Airway Epithelial Cells.

Chlorine Countermeasures: Supplemental Oxygen Equals Supplemental Lung Injury?

β2-Agonists Enhance Asthma-Relevant Inflammatory Mediators in Human Airway Epithelial Cells.

Hypercapnic Acidosis Regulates Mer Tyrosine Kinase Receptor Shedding and Activity.

Biomarkers in Sarcoidosis: Can microRNAs Fill the Gap?

Regulators of G-Protein Signaling as Asthma Therapy?

Inhibition of Macrophage Complement Receptor CRIg by TRIM72 Polarizes Innate Immunity of the Lung.

[Rationale] The complement system plays a critical role in immune responses against pathogens. However, its identity and regulation in the lung are not fully understood. [Objectives] This study aims to explore the role of tripartite motif protein 72 (TRIM72) in regulating complement receptor (CR) of the immunoglobulin superfamily (CRIg) in alveolar macrophage (AM) and innate immunity of the lung. [Methods] Imaging, absorbance quantification and flow cytometry were used to evaluate in vitro and in vivo AM ph...

NO-independent sGC Activation Improves Vascular Function and Cardiac Remodeling in Sickle Cell Disease.

Sickle cell disease (SCD) is associated with intravascular hemolysis and oxidative inhibition of nitric oxide (NO) signaling. BAY 54-6544 is a small molecule activator of oxidized sGC; which unlike endogenous NO and the sGC stimulator BAY 41-8543; preferentially binds and activates heme-free, NO-insensitive sGC to restore enzymatic cGMP production. We tested orally delivered sGC activator BAY 54-6544, sGC stimulator BAY 41-8543, sildenafil, or placebo for 4-12 weeks in a transgenic mouse model of SCD (BERK-...

PDE8 is Expressed in Human Airway Smooth Muscle and Selectively Regulates cAMP Signaling by β2AR-AC6.

Two cAMP signaling compartments centering around adenylyl cyclase (AC) exist in human airway smooth muscle (HASM) cells, one containing ß2AR-AC6 and another containing E prostanoid receptors (EPR)-AC2. We hypothesized that different phosphodiesterase (PDE) isozymes selectively regulate cAMP signaling in each compartment. According to RNA-seq data, 18 of 24 PDE genes were expressed in primary HASM cells derived from age- and gender-matched donors with and without asthma. PDE8A was the third most abundant of...

Characterization of Novel Missense Variants of SERPINA1 Gene Causing Alpha-1 Antitrypsin Deficiency.

SERPINA1 gene is highly polymorphic, with more than one hundred variants described in databases. The SERPINA1 encodes alpha-1 antitrypsin (AAT) protein, and the severe deficiency of AAT is a major contributor to pulmonary emphysema and liver diseases. We report seven new variants in Spanish patients with AAT deficiency. All variants involved amino acid substitutions in different exons: PiSDonosti (S+Ser14Phe), PiTijarafe (Ile50Asn), PiSevilla (Ala58Asp), PiCadiz (Glu151Lys), PiTarragona (Phe227Cys), PiPuert...

PD-1/PD-L1 Pathway Mediates the Alleviation of Pulmonary Fibrosis by Human Mesenchymal Stem Cells in Humanized Mice.

Pulmonary fibrosis is a chronic progressive lung disease with few treatments. Human mesenchymal stem cells (MSC) have been shown to be beneficial to pulmonary fibrosis as they have the immunomodulatory capacity. However, there is no reliable model to test the therapeutic effect of human MSC in vivo.

EphA2 Modulation Associates with Protective Effect of Prone Position in Ventilator-induced Lung Injury.

The erythropoietin-producing hepatoma receptor tyrosine kinase A2 (EphA2) and its ligand ephrinA1 play a pivotal role in inflammation and tissue injury by modulating the epithelial and endothelial barrier integrity. Therefore, EphA2 receptor may be a potential therapeutic target for modulating ventilator-induced lung injury (VILI). To support this hypothesis, here we analyzed EphA2/ephrinA1 signaling in the process of VILI and determined the role of EphA2/ephrinA1 signaling in the protective mechanism of pr...

The Rho Kinase Isoforms ROCK1 and ROCK2 Each Contribute to the Development of Experimental Pulmonary Fibrosis.

Pulmonary fibrosis is thought to result from dysregulated wound repair after repetitive lung injury. Many cellular responses to injury involve rearrangements of the actin cytoskeleton mediated by the two isoforms of the Rho-associated coiled coil forming protein kinase, ROCK1 and ROCK2. Additionally, profibrotic mediators such as transforming growth factor-beta (TGF-β), thrombin and lysophosphatidic acid (LPA) act through receptors that activate ROCK. Inhibition of ROCK activation may be a potent therapeut...

Whole Blood Gene Expression in Pulmonary Non-tuberculous Mycobacterial Infection.

The factors predisposing towards the development of pulmonary non-tuberculous mycobacterial disease (pNTM) and influencing disease progression remain unclear. Impaired immune responses have been reported in individuals with pNTM but data are limited and inconsistent.

Systemic Markers of Adaptive and Innate Immunity are Associated with COPD Severity and Spirometric Disease Progression.

The progression of chronic obstructive pulmonary disease (COPD) is associated with marked alterations in circulating immune cell populations, but no studies have characterized alterations in these cell types across the full spectrum of lung function impairment in current and former smokers. In 6,299 subjects from the COPDGene and ECLIPSE studies, we related Coulter blood counts and proportions to cross-sectional FEV1 adjusting for current smoking status. We also related cell count measures to three-year cha...

Gene-edited MLE-15 Cells as a Model for the Hermansky Pudlak Syndromes.

Defining the mechanisms of cellular pathogenesis for rare lung diseases such as Hermansky Pudlak syndrome (HPS) is often complicated by loss of the differentiated phenotype of cultured primary alveolar type 2 (AT2) cells, and by a lack of durable cell lines that are faithful to both AT2 cell and rare disease phenotypes. We used CRISPR/Cas9 gene editing to generate a series of HPS-specific mutations in the MLE-15 cell line. The resulting MLE-15/HPS cell lines exhibit preservation of AT2 cellular functions, i...

PPARγ Regulates Mitochondrial Structure and Function and HPASMC Proliferation.

Pulmonary hypertension (PH) is a progressive disorder that causes significant morbidity and mortality despite existing therapies. PH pathogenesis is characterized by metabolic derangements that increase pulmonary artery smooth muscle cell (PASMC) proliferation and vascular remodeling. PH-associated decreases in peroxisome proliferator-activated receptor gamma (PPARγ) stimulate PASMC proliferation, and PPARγ in coordination with PPARγ coactivator 1 alpha (PGC1α) regulates mitochondrial gene expression an...

Neutrophil Mediated Suppression of Influenza-induced Pathology Requires CD11b/CD18 (MAC-1).

Severe influenza virus infection can lead to life-threatening pathology through immune-mediated tissue damage. In various experimental models, this damage is dependent on T-cells. There is conflicting evidence regarding the role of neutrophils in influenza-mediated pathology. Neutrophils are often regarded as cells causing tissue damage, but in recent years it has become clear that a subset of human neutrophils is capable of suppressing T-cells, which is dependent on Mac-1 (CD11b/CD18). Therefore, we tested...

FOSL1 Promotes Kras-Induced Lung Cancer Through Amphiregulin and Cell Survival Gene Regulation.

FOSL1/AP-1 transcription factor regulates gene expression controlling various pathophysiological processes. It is a major effector of RAS-ERK1/2 signaling and activated in human lung epithelia by tumorigenic stimuli. Recent evidence shows an inverse correlation between FOSL1 expression and the survival of lung cancer patients with adenocarcinomas; however its role in lung tumorigenesis remains elusive.

Epigenetics of Mucus Hypersecretion in Chronic Respiratory Diseases.

Asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) are three chronic pulmonary diseases that affect an estimated 420 million individuals across the globe. A key factor contributing to each of these conditions is mucus hypersecretion. While management of these diseases is vastly studied, researchers have only begun to scratch the surface of the mechanisms contributing to mucus hypersecretion. Epigenetic regulation of mucus hypersecretion, other than micro RNA (miRNA) post-translat...


Quick Search
Advertisement