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

06:50 EDT 22nd April 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.

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Showing PubMed Articles 1–25 of 373 from American journal of respiratory cell and molecular biology

Angiotensin-(1-7) Attenuated Cigarette Smoking-related Pulmonary Fibrosis via Improving the Impaired Autophagy Caused by NOX4-dependent ROS.

Cigarette smoking is acknowledged as the major risk factor of pulmonary fibrosis. Angiotensin II (Ang II) has been reported to aggravate the smoking-induced lung fibrosis, whereas the effect of angiotensin-(1-7) (Ang-(1-7)) on smoking-related lung fibrosis remains unknown. The autophagy, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of pulmonary fibrosis. However, whether autophagy involves in regulation of smoking-induced lung fibrosis still needs investigation. Here,...

Discoidin Domain Receptor 2 Signaling Regulates Fibroblast Apoptosis Through PDK1/Akt.

Progressive fibrosis is a complication of many chronic diseases and collectively, organ fibrosis is the leading cause of death in the US. Fibrosis is characterized by accumulation of activated fibroblasts and excessive deposition of extracellular matrix proteins, especially type I collagen. Extensive research has supported a role for matrix signaling in propagating fibrosis but type I collagen itself is often considered an end product of fibrosis rather than an important regulator of continued collagen depo...

Hemolysis-induced Lung Vascular Leakage Contributes to the Development of Pulmonary Hypertension.

While hemolytic anemia-associated pulmonary hypertension (PH) and pulmonary arterial hypertension (PAH) are more common than the prevalence of idiopathic PAH alone, the role of hemolysis in the development of PAH is poorly characterized.

Successful Establishment of Primary Type 2 Alveolar Epithelium with 3D Organotypic Co-culture.

Alveolar type 2 (AT2) epithelial cells are uniquely specialized to produce surfactant in the lung and act as progenitor cells in the process of repair after lung injury. AT2 cell injury has been implicated in several lung diseases, including idiopathic pulmonary fibrosis and bronchopulmonary dysplasia. The inability to maintain primary AT2 cells in culture has been a significant barrier in the investigation of pulmonary biology. We have addressed this knowledge gap by developing a 3-dimensional organotypic ...

Epithelial Heparan Sulfate Contributes to Alveolar Barrier Function and is Shed During Lung Injury.

The lung epithelial glycocalyx is a carbohydrate-enriched layer lining the pulmonary epithelial surface. Although epithelial glycocalyx visualization has been reported, its composition and function remain unknown. Using immunofluorescence and mass spectrometry we identified heparan sulfate (HS) and chondroitin sulfate (CS) within the lung epithelial glycocalyx. In vivo selective enzymatic degradation of epithelial HS, but not CS, increased lung permeability. Using mass spectrometry and gel electrophoresis a...

Role of Spdef in the Regulation of Muc5b Expression in the Airways of Naïve and Muco-obstructed Mice.

Understanding how airway secretory mucins MUC5B and MUC5AC expression is regulated in health and disease is important to elucidate the pathogenesis of muco-obstructive respiratory diseases. The transcription factor SPDEF is a key regulator of MUC5AC, but its role in regulating MUC5B in health and in muco-obstructive lung diseases is unknown. Characterization of Spdef-deficient mice upper and lower airways demonstrated region-specific, Spdef-dependent regulation of basal Muc5b expression. Neonatal Spdef-defi...

Amicus or Adversary Revisited: Platelets in Acute Lung Injury & Acute Respiratory Distress Syndrome.

Platelets are essential cellular effectors of hemostasis and contribute to disease as circulating effectors of pathologic thrombosis. These are their most widely known biologic activities. Nevertheless, recent observations demonstrate that platelets have a much more intricate repertoire beyond these traditional functions, and are specialized for contributions to vascular barrier integrity, organ repair, antimicrobial host defense, inflammation, and activities across the immune continuum. Paradoxically, some...

The Microbiome Regulates Pulmonary Responses to Ozone in Mice.

Previous reports demonstrate that the microbiome impacts allergic airway responses, including airway hyperresponsiveness, a characteristic feature of asthma. Here we examined the role of the microbiome in pulmonary responses to a non-allergic asthma trigger, ozone. We depleted the microbiota of conventional mice with either a single antibiotic (ampicillin, metronidazole, neomycin, or vancomycin) or a cocktail of all four antibiotics given via the drinking water. Mice were then exposed to room air or ozone. ...

Early Endotyping - A Chance for Intervention in COPD.

Chronic obstructive pulmonary disease (COPD) is a syndrome that comprises several lung pathologies, but subphenotyping the various disease subtypes has been difficult. One reason may be that current efforts which are focused on studying COPD once it has occurred do not allow to trace back the different origins of disease. This prespective proposes that emphysema originates when susceptible airway, endothelial, and/or hematopoietic cells are exposed to environmental toxins, such as cigarette smoke, biomass f...

Long-term Microevolution of Pseudomonas aeruginosa Differs Between Mildly and Severely Affected Cystic Fibrosis Lungs.

The chronic airway infections with Pseudomonas aeruginosa determine morbidity in most individuals with cystic fibrosis (CF). P. aeruginosa may persist for decades in CF lungs which provides the rare opportunity to study the long-term within-host evolution of a bacterial airway pathogen.

E-cadherin Loss Accelerates Tumor Progression and Metastasis in a Mouse Model of Lung Adenocarcinoma.

Metastatic disease is the primary cause of death of lung cancer patients, but the mouse models of lung adenocarcinoma do not accurately recapitulate the tumor microenvironment or metastatic disease observed in patients. In this study, we conditionally deleted E-cadherin in an autochthonous lung adenocarcinoma mouse model driven by activated oncogenic Kras and p53 loss. Loss of E-cadherin significantly accelerated lung adenocarcinoma progression and decreased survival of the mice. Kras;p53;E-cadherin mice ha...

Genetic Ablation of p16(Ink4a) Does Not Protect Against Cellular Senescence in Mouse Models of COPD/Emphysema.

Cigarette smoke (CS) affects DNA damage and cellular senescence signaling pathways in the pathogenesis of chronic obstructive pulmonary disease (COPD). p16(INK4a) (p16: a cyclin-dependent kinase inhibitor) is a key marker of cellular senescence, which is induced by CS in lung cells. It is thought that removal of p16 attenuates premature aging by removing senesced cells. However, the role of p16 in CS-induced stress induce premature senescence (SIPS) and senescence-associated secretory phenotype (SASP during...

Intermittent Exposure to Cigarette Smoke Increases Lung Tumors and the Severity of Emphysema More Than Continuous Exposure.

Lung cancer and chronic obstructive pulmonary disease (COPD) are leading causes of morbidity and mortality worldwide, and cigarette smoking is a main risk factor for both. The presence of emphysema, an irreversible lung disease, further raises the risk of lung cancer in COPD patients. The mechanisms involved in smoke-induced tumorigenesis and emphysema are not fully understood, attributable to a lack of appropriate animal models. Here, we optimized a model of cigarette smoke (CS)-induced lung cancer and emp...

Involvement of Alveolar Epithelial Cell Necroptosis in IPF Pathogenesis.

Alveolar epithelial cell (AEC) injury leading to cell death is involved in the process of fibrosis development during idiopathic pulmonary fibrosis (IPF). Among regulated/programmed cell death, the excessive apoptosis of AECs has been widely implicated in IPF pathogenesis. Necroptosis is a type of regulated/programmed necrosis. A multiprotein complex composed of receptor-interacting protein kinase-1 and -3 (RIPK1/3) plays a key regulatory role in initiating necroptosis. Although necroptosis participates in ...

TRPV4-stimulation Releases ATP via Pannexin Channels in Human Pulmonary Fibroblasts.

We previously described several ionic conductances in human pulmonary fibroblasts (HPFs), including one activated by two structurally distinct TRPV4-channel agonists: 4α-phorbol-12,13-didecanoate (4αPDD) and GSK1016790A. However, the TRPV4-activated current exhibited peculiar properties: it developed slowly over many minutes, exhibited reversal potentials that could vary by tens of millivolts even within a given cell, and was not easily reversed by subsequent addition of two distinct TRPV4-selective block...

Hypoxia Up-regulates Estrogen Receptor β in Pulmonary Artery Endothelial Cells in a HIF-1α Dependent Manner.

17β-estradiol (E2) attenuates hypoxia-induced pulmonary hypertension (HPH) through estrogen receptor (ER)-dependent effects, including inhibition of hypoxia-induced endothelial cell proliferation; however, the mechanisms responsible remain unknown. We hypothesized the protective effects of E2 in HPH are mediated through hypoxia-inducible factor 1α (HIF-1α)-dependent increases in ERβ expression. Sprague Dawley rats or ERα or ERβ knockout mice were exposed to hypobaric hypoxia for 2-3 weeks. The effects...

Deficient Follistatin-like 3 Secretion by Asthmatic Airway Epithelium Impairs Fibroblast Regulation and Fibroblast-to-myofibroblast Transition.

Bronchial epithelial cells (BECs) from healthy children inhibit human lung fibroblast (HLF) expression of collagen and fibroblast-myofibroblast transition (FMT) while asthmatic BECs do so less effectively, suggesting diminished epithelial-derived regulatory factors contribute to airway remodeling. Preliminary data demonstrated secretion of the activin A-inhibitor FSTL3 by healthy BECs was greater than that by asthmatic BECs.

Upregulation and Nuclear Location of MMP28 in Alveolar Epithelium of Idiopathic Pulmonary Fibrosis.

Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive aging-associated disease of unknown etiology. Growing body of evidence indicates that aberrant activated alveolar epithelial cells induce the expansion and activation of the fibroblast population leading to the destruction of the lung architecture. Some Matrix Metalloproteinases (MMPs) are upregulated in IPF, indicating that they may be important in the pathogenesis and/or progression of IPF. Here, we studied the expression of MMP28 in this di...

Interferon-β Improves Sepsis-related Alveolar Macrophage Dysfunction and Post-septic ARDS-related Mortality.

Interferon-β (IFNβ) is reported to improve survival in patients with acute respiratory distress syndrome (ARDS), possibly by preventing sepsis-induced immunosuppression, but its therapeutic nature in ARDS pathogenesis is poorly understood. We investigated the therapeutic effects of IFNβ for post-septic ARDS to better understand its pathogenesis in mice. Post-septic ARDS was reproduced in mice by cecal ligation and puncture to induce sepsis followed 4 days later by intratracheal instillation of Pseudomona...

Microparticulate Caspase-1 Regulates Gasdermin-D and Pulmonary Vascular Endothelial Cell Injury.

Lung endothelial cell apoptosis and injury occurs throughout all stages of acute lung injury (ALI/ARDS) and impacts disease progression. Caspases 1, 4 and 5 are essential for completion of the apoptotic program known as pyroptosis that also involves pro-inflammatory cytokines.

Platelets Play a Central Role in Sensitization to Allergen.

Platelet activation occurs in patients with allergic inflammation, and platelets can be activated directly by allergen via an IgE-dependent process. Platelets activate antigen-presenting cells (APCs) such as CD11c+ dendritic cells (DCs) in vitro. Whilst CD11c+ DCs are requisite for allergen sensitization, the role of platelets in this process is unknown.

βarrestin-2-dependent Signaling Promotes CCR4-mediated Chemotaxis of Murine T Helper Type 2 Cells.

Allergic asthma is a complex inflammatory disease that leads to significant healthcare costs and reduction in quality of life. Although many cell types are implicated in the pathogenesis of asthma, CD4+ T helper type 2 cells (Th2) are centrally involved. We previously reported that the asthma phenotype is virtually absent in ovalbumin-sensitized and -challenged mice that lack global expression of βarrestin-2 and that CD4+ T cells from these mice displayed significantly reduced C-C motif chemokine 22 (CCL22...

Digital Image Analyses on Whole Lung Slides in Mouse Models of Acute Pneumonia.

Descriptive histopathology of mouse models of pneumonia is essential in assessing the outcome of infections, molecular manipulations or therapies in the context of whole lungs. Quantitative comparisons between experimental groups, however, have been limited to laborious stereology or ill-defined scoring systems that depend on the subjectivity of a more or less experienced observer. Here, we introduce self-learning digital image analyses that allow to transform optical information from whole mouse lung secti...

Riboflavin Metabolism Variation Among Clinical Isolates of Streptococcus pneumoniae Results in Differential Activation of MAIT Cells.

Streptococcus pneumoniae is an important bacterial pathogen that causes a range of non-invasive and invasive diseases. The mechanisms underlying variability in the ability of S. pneumoniae to transition from nasopharyngeal colonization to disease-causing pathogen are not well-defined. Mucosal-associated invariant T (MAIT) cells are prevalent in mucosal tissues such as the airways and are thought to play an important role in the early response to infection with bacterial pathogens. The ability of MAIT cells ...

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 ...


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