Pulmonary Cell News Volume 2.50 | Dec 19 2013

Arsenic Compromises Conducting Airway Epithelial Barrier Properties in Primary Mouse and Immortalized Human Cell Cultures
To quantify arsenic-induced changes in tight junction transmembrane proteins, researchers conducted arsenic exposure experiments with an immortalized human bronchial epithelial cell line (16HBE14o-). They found that arsenic exposure significantly increased the protein expression of Cl-4 and occludin as well as the mRNA levels of Cl-4 and Cl-7 in these cells. [PLoS One] Full Article

Proinflammatory Effects and Oxidative Stress within Human Bronchial Epithelial Cells Exposed to Atmospheric Particulate Matter (PM2.5 and PM>2.5) Collected from Cotonou, Benin
Researchers conducted a complete physicochemical characterization of PM2.5 and PM>2.5 after particulate matter (PM) collection in Cotonou (Benin). Adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations to determine global cytotoxicity. [Environ Pollut] Abstract

Effect of Epithelium ATP Release on Cyclic Pressure-Induced Airway Mucus Secretion
Scientists evaluated the effect of adenosine triphosphate (ATP) release from and intracellular calcium in epithelial cells on cyclic pressure-induced mucus secretion in the airway. Human bronchial epithelial cells (16HBE) were cultured in vitro on cyclically tilted cultured plates and divided into five groups: control, tilt, tilt and BAPTA-AM, tilt and EGTA, and tilt and RB-2. [Biosci Rep] Abstract | Full Article

LUNG CANCER

mTOR-Dependent Transcriptional Repression of Pdcd4 Tumor Suppressor in Lung Cancer Cells
The authors investigated the molecular mechanisms of Programmed cell death 4 (Pdcd4) suppression in lung cancer cells. Besides enhanced mTOR-dependent proteasomal degradation of Pdcd4 protein, they found that Pdcd4 transcription is negatively regulated by mTOR signaling, and localized cis-acting element in Pdcd4 promoter responsible for this effect. [Biochim Biophys Acta] Abstract

Improved Apoptotic Cell Death in Drug-Resistant Non Small Cell Lung Cancer Cells by TRAIL-Based Treatment
Since response to platinum-based therapy in non small cell lung cancer is poor, the present study was designed to rationally identify novel drug combinations in cell models including the A549 cell line and the cisplatin-resistant subline A549/Pt, characterized by reduced sensitivity to cisplatin-induced apoptosis and by up-regulation of efflux transporters of the ATP binding cassette superfamily. [J Pharmacol Exp Ther]
Abstract | Full Article

Resistance to ROS1 Inhibition Mediated by EGFR Pathway Activation in Non-Small Cell Lung Cancer
The authors sought to determine mechanisms of acquired resistance to ROS1 inhibition. To accomplish this, they analyzed non-small cell lung cancer (NSCLC) tumor samples from a patient who initially responded to the ROS1 inhibitor crizotinib but eventually developed acquired resistance. In addition, they generated a ROS1 inhibition-resistant derivative of the initially sensitive NSCLC cell line HCC78. [PLoS One] Full Article

Acquisition of Epithelial-Mesenchymal Transition Phenotype and Cancer Stem Cell-Like Properties in Cisplatin-Resistant Lung Cancer Cells through AKT/β-Catenin/Snail Signaling Pathway
Researchers showed that cisplatin-resistant A549 cells acquire epithelial-mesenchymal transition phenotype associated with migratory and invasive capability. Cisplatin- resistant A549 cells also displayed enhanced cancer stem cell-like properties. [Eur J Pharmacol] Abstract

The Mitochondrial Cyclophilin D/p53 Complexation Mediates Doxorubicin-Induced Non-Apoptotic Death of A549 Lung Cancer Cells
Doxorubicin has displayed significant cytotoxic effects against lung cancer cells; however, the underlying mechanisms remain inconclusive. Researchers provide evidence that mitochondrial p53 and cyclophilin D complexation is required for doxorubicin-induced death of lung cancer A549 cells. [Mol Cell Biochem] Abstract

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The Pulmonary Fibrosis Community Again Commends The Pulmonary Fibrosis Foundation’s Biennial PFF Summit
The Pulmonary Fibrosis Foundation (PFF) presented its second biennial healthcare conference, PFF Summit 2013: From Bench to Bedside, in La Jolla, California, from December 5-7, 2013. The innovative conference brought together medical professionals, patients, and caregivers for a three-day meeting. Over 520 people, including individuals from 16 countries, attended the PFF Summit 2013. [Pulmonary Fibrosis Foundation]
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Postdoctoral Position – Pulmonary Research (The Ohio State University College of Pharmacy)

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Assistant Professor, Associate Professor, Professor – Lung Biology or Pulmonary and Critical Care Diseases (Boston University School of Medicine & Boston Medical Center)

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PhD Position – Genetics of Non-Smoker Chronic Obstructive Pulmonary Disorders (Göttingen Center for Molecular Biosciences)

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Research Associate/Scientist – Antibodies Group (STEMCELL Technologies Inc.)

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