Adiponectin (Acrp30) is an insulin-sensitizing fat hormone that has enormous potential as a therapeutic target for obesity-related diseases, including diabetes, atherosclerosis and cancer. More- over, it displays anti-inflammatory actions and attenuates inflam- matory responses in several tissues and cell cultures. It has been reported elevated serum levels of Acrp30 in Chronic Obstructive Pulmonary disease (COPD) patients but the role of the increased levels are not yet clarified. Since COPD patients are characterized by increased serum and sputum concentrations of several cyto- kines (TNFa, IL-6, IL-1b), in this study we analyzed the effects of Acrp30 treatment in A549 cells (human lung adenocarcinoma) selected as a in vitro model of lung epithelia. Furthermore, we investigated the role of Acrp30 at two concentrations (5 and 50 lg/ml) in A549 cells treated with TNFa. We performed a via- bility assay (MTT test) and demonstrated that Acrp30 reduces cell viability in a dose and time dependent manner; interestingly in pre-treated cells with pro-inflammatory cytokine TNFa, Acrp30 treatment (48 and 72 hours) is able to ameliorate the pro- liferation rate. We found also that the reduction of cell viability induced by Acrp30 is linked to the inhibition in ERK1/2 phos- phorylation and that the beneficial effects induced in co-treat- ment with cytokines is mediated by activation in ERK1/2 phosphorylation. Our data show that Acrp30 could play a central role in the con- trol of local lung inflammatory state and epithelial cell degenera- tion in lung of COPD patients, thus Acrp30 may represent a target for the development of new therapeutic approaches also in inflammatory diseases as COPD, an increasing global health problem

Adiponectin is involved in the control of human lung epithelial A549 cell viability

Nigro E;BIANCO, Andrea;DANIELE, Aurora
2011

Abstract

Adiponectin (Acrp30) is an insulin-sensitizing fat hormone that has enormous potential as a therapeutic target for obesity-related diseases, including diabetes, atherosclerosis and cancer. More- over, it displays anti-inflammatory actions and attenuates inflam- matory responses in several tissues and cell cultures. It has been reported elevated serum levels of Acrp30 in Chronic Obstructive Pulmonary disease (COPD) patients but the role of the increased levels are not yet clarified. Since COPD patients are characterized by increased serum and sputum concentrations of several cyto- kines (TNFa, IL-6, IL-1b), in this study we analyzed the effects of Acrp30 treatment in A549 cells (human lung adenocarcinoma) selected as a in vitro model of lung epithelia. Furthermore, we investigated the role of Acrp30 at two concentrations (5 and 50 lg/ml) in A549 cells treated with TNFa. We performed a via- bility assay (MTT test) and demonstrated that Acrp30 reduces cell viability in a dose and time dependent manner; interestingly in pre-treated cells with pro-inflammatory cytokine TNFa, Acrp30 treatment (48 and 72 hours) is able to ameliorate the pro- liferation rate. We found also that the reduction of cell viability induced by Acrp30 is linked to the inhibition in ERK1/2 phos- phorylation and that the beneficial effects induced in co-treat- ment with cytokines is mediated by activation in ERK1/2 phosphorylation. Our data show that Acrp30 could play a central role in the con- trol of local lung inflammatory state and epithelial cell degenera- tion in lung of COPD patients, thus Acrp30 may represent a target for the development of new therapeutic approaches also in inflammatory diseases as COPD, an increasing global health problem
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11591/168744
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