Decreased phosphatase PTEN amplifies PI3K signaling and enhances proinflammatory cytokine release in COPD

American Journal of Physiology. Lung Cellular and Molecular Physiology
Satoru YanagisawaPeter J Barnes

Abstract

The phosphatidylinositol 3-kinase (PI3K) pathway is activated in chronic obstructive pulmonary disease (COPD), but the regulatory mechanisms for this pathway are yet to be elucidated. The aim of this study was to determine the expression and role of phosphatase and tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the PI3K pathway, in COPD. PTEN protein expression was measured in the peripheral lung of COPD patients compared with smoking and nonsmoking controls. The direct influence of cigarette smoke extract (CSE) on PTEN expression was assessed using primary lung epithelial cells and a cell line (BEAS-2B) in the presence or absence of l-buthionine-sulfoximine (BSO) to deplete intracellular glutathione. The impact of PTEN knockdown by RNA interference on cytokine production was also examined. In peripheral lung, PTEN protein was significantly decreased in patients with COPD compared with the subjects without COPD (P < 0.001) and positively correlated with the severity of airflow obstruction (forced expiratory volume in 1-s percent predicted; r = 0.50; P = 0.0012). Conversely, phosphorylated Akt, as a marker of PI3K activation, showed a negative correlation with PTEN protein levels (r = -0.41; P = 0.0042...Continue Reading

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Citations

Jan 20, 2018·American Journal of Physiology. Lung Cellular and Molecular Physiology·Zhen XiaoYong Han
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Oct 5, 2018·American Journal of Physiology. Lung Cellular and Molecular Physiology·Brendan Mallia-MilanesSimon R Johnson
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Nov 2, 2019·American Journal of Respiratory Cell and Molecular Biology·Ion CristóbalJesús García-Foncillas
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Methods Mentioned

BETA
transfection
protein
phosphatase assay
PCR
ELISA

Software Mentioned

Statcel

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