Volume 4.23 | Jun 18

Pulmonary Cell News 4.23 June 18, 2015
Pulmonary Cell News
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Streptococcus pneumoniae Secretes Hydrogen Peroxide Leading to DNA Damage and Apoptosis in Lung Cells
Investigators showed that S. pneumoniae induces toxic DNA double-strand breaks in human alveolar epithelial cells, as indicated by ataxia telangiectasia mutated kinase-dependent phosphorylation of histone H2AX and colocalization with p53-binding protein. [Proc Natl Acad Sci USA] Abstract | Full Article
Learn More: Model the Human Airway at the Air-Liquid Interface
PUBLICATIONS (Ranked by impact factor of the journal)
Virulence Factors of Pseudomonas aeruginosa Induce Both the Unfolded Protein and Integrated Stress Responses in Airway Epithelial Cells
The authors showed that cell-free conditioned medium of the PAO1 strain of P. aeruginosa, containing secreted virulence factors, induces endoplasmic reticulum stress in primary bronchial epithelial cells as evidenced by splicing of XBP1 mRNA and induction of CHOP, GRP78 and GADD34 expression. [PLoS Pathog] Full Article

Morphine Compromises Bronchial Epithelial TLR2/IL17R Signaling Crosstalk, Necessary for Lung IL17 Homeostasis
Researchers showed that early induction of IL17 from the bronchial epithelium, following pathogenic encounter is a protective response, which contributes to pathogenic clearance and currently attributed to TLR2 activation in immune cells. [Sci Rep] Full Article

Aryl Hydrocarbon Receptor Agonists Upregulate VEGF Secretion from Bronchial Epithelial Cells
By treating HBE-135, Beas-2B, and primary human bronchial epithelial cells (BECs) with aryl hydrocarbon receptor (AhR) agonists, the mechanisms through which AhR modulated vascular endothelial growth factor (VEGF) expression in human BECs were investigated. [J Mol Med] Abstract

Aspergillus fumigatus Activates PAR-2 and Skews Toward a Th2 Bias in Airway Epithelial Cells
Researchers tested the hypothesis that A. fumigatus (AF) can modulate the response of airway epithelial cells to favor a Th2 response. Exposure of bronchial epithelial cells to AF extract suppressed poly I:C and HRV16 signaling via PAR-2 activation. [Am J Respir Cell Mol Biol] Abstract

Fibroblast-Epithelial Cell Interactions Drive Epithelial-Mesenchymal Transition Differently in Cells from Normal and COPD Patients
Scientists investigated the hypothesis that epithelial-to-mesenchymal transition (EMT) is active in human bronchial epithelial cells of chronic obstructive pulmonary disease (COPD) patients, and that mediators secreted by lung fibroblasts from COPD patients induce EMT. [Respir Res] Abstract | Full Article


A Non-Tight Junction Function of Claudin-7—Interaction with Integrin Signaling in Suppressing Lung Cancer Cell Proliferation and Detachment
Claudin-7 co-localizes and forms a stable complex with integrin β1. Both suppressing claudin-7 expression by lentivirus shRNA in human lung cancer cells and deletion of claudin-7 in mouse lungs lead to the reduction in integrin β1 and phospho-FAK levels. [Mol Cancer] Full Article

Novel EPHB4 Receptor Tyrosine Kinase Mutations and Kinomic Pathway Analysis in Lung Cancer
Scientists reported the identification of novel EPHB4 mutations that lead to putative structural alterations as well as increased cellular proliferation and motility. They showed that EPHB4 mutations can induce broad changes in the kinome signature of lung cancer cells. [Sci Rep] Full Article

Genetic and Functional Analysis of Polymorphisms in the Human Dopamine Receptor and Transporter Genes in Small Cell Lung Cancer
Cell treatment with the dopamine (DA) D1 receptor antagonist SCH23390 inhibited SKF38393 effects. In contrast, the DA D2 receptor agonist quinpirole counteracted, in a dose and time dependent way, small cell lung cancer cell proliferation, it did not affect cAMP levels and decreased phosphorylated AKT that was induced by DA D2 receptor antagonist sulpiride. [J Cell Physiol] Abstract

Epigenetic Regulation of miR-129-2 and Its Effects on the Proliferation and Invasion in Lung Cancer Cells
To investigate whether DNA methylation alters the expression of microRNA (miR)-129 in lung cancer, scientists performed DNA methylation assays and found that 5′ untranslated region of miR-129-2 gene was absolutely methylated in both A549 and SPCA-1 lung cancer cells, but totally un-methylated in 95-D cells. [J Cell Mol Med] Full Article

Sanguinarine-Induced Apoptosis in Lung Adenocarcinoma Cells Is Dependent on Reactive Oxygen Species Production and Endoplasmic Reticulum Stress
The authors explored the anticancer properties of sanguinarine (SAN) in lung cancer using the human lung adenocarcinoma cell line SPC-A1. They revealed that SAN inhibited SPC-A1 cell growth and induced apoptosis in a dose-dependent manner. [Oncol Rep] Abstract

Going to ISSCR 2015? We’ll see you there!
Airway Hydration and COPD
The authors highlight the cellular components responsible for maintaining mucociliary clearance (MCC) and how this process is disrupted following tobacco exposure and with chronic bronchitis. They also discuss existing therapeutic strategies for the treatment of chronic bronchitis and how components of the MCC can be used as biomarkers for the evaluation of tobacco or tobacco-like-product exposure. [Cell Mol Life Sci] Abstract

Visit our reviews page to see a complete list of reviews in the pulmonary cell research field.

4th Annual Excellence in Lung Cancer Screening & Continuum of Care
Mayo Clinic and United Therapeutics Collaborate on Lung Restoration Center
Mayo Clinic in Jacksonville, Florida, and United Therapeutics Corporation announced a collaboration to build and operate a lung restoration center on the Mayo campus. [Mayo Clinic] Press Release

Ventana Receives FDA Approval for the First Fully Automated IHC Companion Diagnostic to Identify Lung Cancer Patients Eligible for XALKORI® (Crizotinib)
Ventana Medical Systems, Inc. announced approval of the VENTANA ALK CDx Assay by the US Food and Drug Administration (FDA) as a companion diagnostic to aid in the identification of patients for Pfizer’s FDA approved targeted therapy, XALKORI®. [Ventana Medical Systems, Inc.] Press Release

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$13 Million More for Lung Cancer Research
The House of Representatives passed the FY16 Department of Defense Appropriations Bill. This legislation includes $13 million for lung cancer research under the Congressionally Directed Medical Research Program bringing the total funding to $102 million. [Lung Cancer Alliance] Editorial

National Institutes of Health (United States)

Food and Drug Administration (United States)

Center for Biologics Evaluation and Research (United States)

European Medicines Agency (European Union)

Medicines and Healthcare Products Regulatory Agency (United Kingdom)

Therapeutic Goods Administration (Australia)
NEW 3rd Annual International Conference on Advances in Medical Research (CAMR 2015)
August 17-18, 2015
Singapore, Singapore

Visit our events page to see a complete list of events in the pulmonary cell community.
NEW Senior Scientist – Stem Cells (Cystic Fibrosis Foundation)

NEW Faculty Positions (Cleveland Clinic)

NEW Postdoctoral Position – Lung Myofibroblasts and Fibrosis (Yale University School of Medicine)

Scientist – Pluripotent Stem Cell Biology Endoderm Lineages (STEMCELL Technologies Inc.)

Research Scientist I/II – Fibrosis/Oncology/Inflammation Biology (Gilead Sciences)

Medical Professional – Molecular Genetic Pathology (Paris Est Créteil)

Postdoctoral Research Fellow – Lung Transplant Immunology (Washington University)

Senior PostDoc/Research Group Leader – Chronic Lung Disease (Ludwig Boltzmann Institute for Lung Vascular Research)

Postdoctoral Researcher – Pulmonary Developmental Pathology (Drexel University College of Medicine)

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