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Adipose Derived Mesenchymal Stem Cell Therapy Is Comparable or Superior to Bone-Marrow Derived on Hypoxia-Induced Lung Injury in Primary Rat Alveolar Epithelial Cells
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A2253 - Adipose Derived Mesenchymal Stem Cell Therapy Is Comparable or Superior to Bone-Marrow Derived on Hypoxia-Induced Lung Injury in Primary Rat Alveolar Epithelial Cells
Author Block: N. Shologu1, D. O'Toole1, M. Scully2, J. G. Laffey1; 1Discipline of Anaesthesia and Lung Biology Group, National University of Ireland Galway, Galway, Ireland, 2Critical Care Medicine and Intensive Care, University Hospital Galway, Galway, Ireland.
Introduction: Pulmonary ischemia reperfusion injury occurs during major surgical procedures and organ transplantation. During ischemia, oxygen deprivation directly generates oxidative tissue damage and hypoxia, followed by reperfusion which results in the upregulation of inflammatory mediators, oedema, and pulmonary infiltrates. Hypoxia contributes to lung injury by triggering a series of events following in variable degrees of cellular damage and activation of cytotoxic mediators, eventually culminating in cell death. Aim of the study: To investigate the modulation of inflammatory response, oxidative stress, and intrinsic and extrinsic factors driving the protective effects of mesenchymal stem cells (MSC) therapy in alveolar type II (ATII) cells, and their effect on a hypoxia-induced injury model. Material and Methods: MSC-conditioned media (CM) was prepared from confluent human bone marrow or adipose derived MSC cultures. Primary ATII cells isolated from rat lungs were treated with MSC-CM then subjected to hypoxia for 24 h, cell viability, apoptosis and necrosis were assessed via MTT assay, and FACS. Several factors of the inflammatory response, inhibition of reactive oxygen species (ROS) expression, and the involvement of the mitogen-activated protein kinase (MAPK) pathways were investigated by ELISA, DCF assay, and Western blot, respectively. Results: In comparison to normoxic control, ROS generation and caspase 3 release were increased in hypoxic control while both MSC-CM attenuated these effects. Both inhibition of MAPK pathways, and endoplasmic reticulum (ER) stress mediators led to increased hypoxia-induced apoptosis and necrosis. Reduced levels of pro-inflammatory cytokines and increased levels of anti-inflammatory mediators were observed in MSC-CM treated group compared to hypoxic control. Conclusion: Together, these findings suggest predominance of the MAPK pathways and ER stress mediators in the protective effect of MSC therapy in lung injury induced by hypoxia.
Author Block: N. Shologu1, D. O'Toole1, M. Scully2, J. G. Laffey1; 1Discipline of Anaesthesia and Lung Biology Group, National University of Ireland Galway, Galway, Ireland, 2Critical Care Medicine and Intensive Care, University Hospital Galway, Galway, Ireland.
Introduction: Pulmonary ischemia reperfusion injury occurs during major surgical procedures and organ transplantation. During ischemia, oxygen deprivation directly generates oxidative tissue damage and hypoxia, followed by reperfusion which results in the upregulation of inflammatory mediators, oedema, and pulmonary infiltrates. Hypoxia contributes to lung injury by triggering a series of events following in variable degrees of cellular damage and activation of cytotoxic mediators, eventually culminating in cell death. Aim of the study: To investigate the modulation of inflammatory response, oxidative stress, and intrinsic and extrinsic factors driving the protective effects of mesenchymal stem cells (MSC) therapy in alveolar type II (ATII) cells, and their effect on a hypoxia-induced injury model. Material and Methods: MSC-conditioned media (CM) was prepared from confluent human bone marrow or adipose derived MSC cultures. Primary ATII cells isolated from rat lungs were treated with MSC-CM then subjected to hypoxia for 24 h, cell viability, apoptosis and necrosis were assessed via MTT assay, and FACS. Several factors of the inflammatory response, inhibition of reactive oxygen species (ROS) expression, and the involvement of the mitogen-activated protein kinase (MAPK) pathways were investigated by ELISA, DCF assay, and Western blot, respectively. Results: In comparison to normoxic control, ROS generation and caspase 3 release were increased in hypoxic control while both MSC-CM attenuated these effects. Both inhibition of MAPK pathways, and endoplasmic reticulum (ER) stress mediators led to increased hypoxia-induced apoptosis and necrosis. Reduced levels of pro-inflammatory cytokines and increased levels of anti-inflammatory mediators were observed in MSC-CM treated group compared to hypoxic control. Conclusion: Together, these findings suggest predominance of the MAPK pathways and ER stress mediators in the protective effect of MSC therapy in lung injury induced by hypoxia.
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