Pulmonary Cell News Volume 3.05 | Feb 13 2014

Antifibrotic Effects of Noscapine through Activation of Prostaglandin E2 Receptors and Protein
Kinase A
Researchers examined the potential antifibrotic effects of the antitussive drug, noscapine, recently found to bind microtubules and affect microtubule dynamics. Noscapine did not activate protein kinase A in human bronchial or alveolar epithelial cells. [J Biol Chem] Abstract | Full Article

Cigarette Smoke-Induced Alveolar Epithelial-Mesenchymal Transition Is Mediated by Rac1 Activation
Epithelial-mesenchymal transition was induced in mice and pulmonary epithelial cells by exposure of cigarette smoke and cigarette smoke extract (CSE) respectively. Treatment of pulmonary epithelial cells with CSE elevated Rac1 expression associated with increased TGF-ß1 release. [Biochim Biophys Acta] Abstract

Activation of Transcription Factor Nrf2 Signaling by the Sphingosine Kinase Inhibitor SKI-II Is Mediated by the Formation of Keap1 Dimers
Nuclear factor erythroid 2-related factor 2 (Nrf2) was stabilized by SKI-II (2-(p-hydroxyanilino)-4-(p-chlorophenyl) thiazole), which is a known sphingosine kinase inhibitor, in the human bronchial epithelial cell line, BEAS2B, and in primary human bronchial epithelial cells, leading to enhancement of anti-oxidant proteins, such as HO-1, NQO1 and GCLM. [PLoS One] Full Article

Activated Alveolar Epithelial Cells Initiate Fibrosis through Autocrine and Paracrine Secretion of Connective Tissue Growth Factor
Scientists found that alveolar epithelial cells undergoing TGFß-mediated mesenchymal transition in vitro were also capable of activating lung fibroblasts through production of connective tissue growth factor. [Am J Physiol Lung Cell Mol Physiol] Abstract

mTOR Inhibition of Cardamonin on Antiproliferation of A549 Cells Is Involved in a FK506 Binding Protein Independent Fashion
The antiproliferative effect and the possible mechanism of combining with mammalian target of rapamycin (mTOR) of cardamonin were investigated on A549 cells. Treated with cardamonin, the proliferation of A549 cells was inhibited. [Life Sci] Abstract

LUNG CANCER

MicroRNA-545 Suppresses Cell Proliferation by Targeting Cyclin D1 and CDK4 in Lung Cancer Cells
Researchers found that microRNA (miR)-545 was less abundant in cancerous lung tissues than in adjacent non-cancerous tissues. Further studies showed that miR-545 suppressed cell proliferation in vitro and in vivo. [PLoS One] Full Article

PKCd/Midkine Pathway Drives Hypoxia-Induced Proliferation and Differentiation of Human Lung Epithelial Cells
Replication of human lung epithelial cells was significantly increased by chronic hypoxia and was dependent on expression of protein kinase C (PKC)d. Hypoxia-induced proliferation of epithelial cells was accompanied by translocation of PKCd from Golgi into the nuclei. [Am J Physiol Lung Cell Mol Physiol] Abstract

Microvesicle-Associated MicroRNA Expression Is Altered upon Particulate Matter Exposure in Healthy Workers and in A549 Cells
Scientists evaluated expression of microRNAs (miR) contained within plasma microvesicles (MVs) upon particulate matter (PM) exposure both in vivo and in vitro. In vitro experiments confirmed a dose-dependent expression of miR-128 in MVs released from A549 cells after six?hours of PM treatment. [J Appl Toxicol]
Full Article

Propofol Induces Endoplasmic Reticulum (ER) Stress and Apoptosis in Lung Cancer Cell H460
Researchers demonstrated the effects of propofol on the proliferation and the apoptosis of lung cancer cell H460 by using colony formation assay and flow cytometry. [Tumor Biol] Abstract

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Ario Pharma Commences Phase IIa Trial of TRPV1 Inhibitor for Cough Associated with Chronic Obstructive Pulmonary Disease
Ario Pharma Ltd announced that it has commenced a Phase IIa study of its TRPV1 antagonist, XEN-0501, for the treatment and prevention of cough in patients with chronic obstructive pulmonary disease. [Ario Pharma Ltd] Press Release

Director of Women’s Guild Lung Institute Awarded Stem Cell Grant to Study Treatment for Lung Disease
A Cedars-Sinai research team led by Paul W. Noble, MD, chair of the Department of Medicine and director of the Women’s Guild Lung Institute, has been awarded $628,816 by California’s stem cell agency to develop a treatment for idiopathic pulmonary fibrosis, a deadly disease that destroys the lungs and damages other vital organs. [Cedars-Sinai] Press Release

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NEW Research Technologist – Pluripotent Stem Cells (STEMCELL Technologies Inc.)

NEW Research Technologist – Particle Chemistry (STEMCELL Technologies Inc.)

NEW Research Technologist – PSC Biology and Bioengineering (STEMCELL Technologies Inc.)

Postdoctoral Research Fellow – Lung Cancer Genetics (Fred Hutchinson Cancer Research Center)

Research Associate (Assistant Professor) – Pulmonary Medicine (University of Chicago)

PhD Studentships in Pulmonary Medicine (University of Giessen and Marburg Lung Center)

Chair in Lung Cancer Research (The University of Manchester)

Postdoctoral Scholar – Molecular Mechanisms of Lung Cancer, Lung Regeneration and Lung Development (UCSF)

Postdoctoral Position – Metabolomics of Pulmonary Medicine (Karolinska Institute)

Postdoctoral Fellow – Role of Stem Cells in Chronic Lung Disease (MedImmune)

Postdoctoral Research Fellow – Lung Development, Injury/Repair and Fibrosis (Mayo Clinic)

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