Pulmonary Cell News Volume 3.30 | Aug 7 2014

Mitophagy-Dependent Necroptosis Contributes to the Pathogenesis of COPD
The pathogenesis of chronic obstructive pulmonary disease (COPD) remains unclear, but involves loss of alveolar surface area and airway inflammation as the consequence of cigarette smoke (CS) exposure. Using cultured pulmonary epithelial cells and murine models, investigators demonstrate that CS causes mitochondrial dysfunction that is associated with a reduction of mitochondrial membrane potential. [J Clin Invest] Full Article

Alpha-Klotho Protects against Oxidative Damage in Pulmonary Epithelia
Heterozygous alpha-Klotho (αKlotho) haplo-insufficient mice appear normal at baseline except for age-related changes in the lung, suggesting heightened pulmonary susceptibility to αKlotho deficiency. Investigators used in vivo and in vitro models to test whether αKlotho protects lung epithelia against injury. [Am J Physiol Lung Cell Mol Physiol] Abstract

Human CD56⁺ Cytotoxic Lung Lymphocytes Kill Autologous Lung Cells in Chronic Obstructive Pulmonary Disease
Lung CD56⁺ lymphocytes, but not CD4⁺ or CD8⁺ conventional lung T cells, rapidly killed autologous lung cells without additional stimulation. Such natural cytotoxicity was increased in subjects with severe chronic obstructive pulmonary disease and was unexplained in multiple regression analysis by age or cancer as indication for surgery. [PLoS One] Full Article

Interaction of Alveolar Epithelial Cells with CFP21, a Mycobacterial Cutinase-Like Enzyme
Scientists hypothesized that culture filtrate protein 21 (CFP21) could be playing a role in Mycobacterium tuberculosis virulence by disrupting the host cell integrity. The in vitro exposure of type I and type II alveolar epithelial cells to CFP21 resulted in a significant decline in their cellular viability by inducing cell apoptosis. [Mol Cell Biochem] Abstract

LUNG CANCER

p53ψ Is a Transcriptionally Inactive p53 Isoform Able to Reprogram Cells toward a Metastatic-Like State
Like certain p53 gain-of-function mutants, p53ψ attenuates the expression of E-cadherin, induces expression of markers of the epithelial-mesenchymal transition, and enhances the motility and invasive capacity of cells through a unique mechanism involving the regulation of cyclophilin D activity, a component of the mitochondrial inner pore permeability. [Proc Natl Acad Sci USA] Abstract | Full Article | Press Release

Anti-Cancer Effect of Tectochrysin in NSCLC Cells through Overexpression of Death Receptor and Inactivation of STAT3
Investigators focused on the anticancer effects of tectochrysin on human non-small-cell lung cancer (NSCLC) cells and its mechanism of action. They analyzed the activity of tectochrysin on NSCLC cells by use of Western blot analysis for major apoptotic proteins and death receptor expression. [Cancer Lett] Abstract

Rho GTPases RhoA and Rac1 Mediate Effects of Dietary Folate on Metastatic Potential of A549 Cancer Cells through the Control of Cofilin Phosphorylation
Scientists have previously shown that the withdrawal of media folate leads to the inhibition of migration and invasion of A549 lung carcinoma cells. Now they demonstrate that media folate regulates the function of Rho GTPases by enabling their carboxyl methylation and translocation to plasma membrane. [J Biol Chem]
Abstract | Full Article

Pharmacological Modulation of Autophagy Enhances Newcastle Disease Virus-Mediated Oncolysis in Drug-Resistant Lung Cancer Cells
The effect of Newcastle disease virus (NDV) strain NDV/FMW infection on autophagy machinery in A549 lung cancer cell lines resistant to cisplatin or paclitaxel was investigated by detection of GFP-microtubule-associated protein 1 light chain 3 puncta, formation of double-membrane vesicles and conversion of the nonlipidated form of LC3 to the phosphatidylethanolamine-conjugated form. [BMC Cancer] Abstract | Full Article

Cancer Cell Growth Inhibitory Effect of Bee Venom via Increase of Death Receptor 3 Expression and Inactivation of NF-Kappa B in NSCLC Cells
Previous findings have demonstrated that bee venom (BV) has anti-cancer activity in several cancer cells. Researchers found BV inhibited growth of lung cancer cells by induction of apoptosis in a dose dependent manner in lung cancer cell lines A549 and NCI-H460. Consistent with apoptotic cell death, expression of DR3 and DR6 was significantly increased. [Toxins] Full Article

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Boehringer Ingelheim Receives Two FDA Approvals
Boehringer Ingelheim announced the U.S. Food and Drug Administration (FDA) approved two different chronic obstructive pulmonary disease products at the end of last week. [Boehringer Ingelheim GmbH] Press Release

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Postdoctoral Scientist – Transcriptional Networks in Lung Cancer (Cancer Research UK Manchester Institute)

Postdoctoral Fellowship – Molecular Biology (Wayne State University)

Postdoctoral Fellow – Mechanisms of Lung Alveoli Epithelial Repair (University of Illinois Chicago College of Medicine)

Postdoctoral Research Associate – Lung Development Research (Women and Infants Hospital of Rhode Island)

Postdoctoral Research Trainee – Lung Injury and Epithelial Repair (University of Tennessee Health Science Center)

Postdoctoral Scholar – Molecular Mechanisms of Lung Cancer, Lung Regeneration and Lung Development (University of California – San Francisco)

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

Scientist – Pluripotent Stem Cell Media Development, High Throughput Screening (STEMCELL Technologies Inc.)

Scientist – Cell Culture Support Products (STEMCELL Technologies Inc.)

Scientist – Immunology/Cell Separation (STEMCELL Technologies Inc.)

Research Associate – Cell Separation (STEMCELL Technologies Inc.)

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