Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation
Ventilator-induced lung injury (VILI) is a common complication that results from treatment with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS) patients. The present study investigated the effect of endothelial progenitor cell (EPC) transplantation on VILI. Wistar rats were...
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doaj-a85c72cedd3743c58585657d411936042021-03-24T11:33:19ZengSAGE PublishingCell Transplantation0963-68971555-38922019-12-012810.1177/0963689719874048Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume VentilationYing-nan Ju0Ying-jie Geng1Xue-ting Wang2Jing Gong3Jingli Zhu4Wei Gao5 Department of Intensive Care Unit, The Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China Department of Anesthesiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, ChinaVentilator-induced lung injury (VILI) is a common complication that results from treatment with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS) patients. The present study investigated the effect of endothelial progenitor cell (EPC) transplantation on VILI. Wistar rats were divided into three groups ( n = 8): sham (S), VILI model (V) induced by tidal volume ventilation (17 mL/kg), and VILI plus EPC transplantation (VE) groups. The lung PaO 2 /FiO 2 ratio, pulmonary wet-to-dry (W/D) weight ratio, number of neutrophils, total protein, neutrophil elastase level, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were examined. Furthermore, the histological and apoptotic analysis, and lung tissue protein expression analysis of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase (MMP)-9, total nuclear factor kappa B (total-NF-κB), phosphorylated NF-κB (phospho-NF-κB) and myosin light chain (MLC) were performed. The ventilation-induced decrease in PaO 2 /FiO 2 ratio, and the increase in W/D ratio and total protein concentration were prevented by the EPC transplantation. The EPC transplantation (VE group) significantly attenuated the VILI-induced increased expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8, MMP-9, phospho-NF-κB and MLC, neutrophil elastase levels and neutrophil counts in BALF. In addition, the anti-inflammatory factor IL-10 increased in the VE group. Furthermore, pulmonary histological injury and apoptosis (TUNEL-positive cells, increase in Bax and cleaved caspase-3) were considerably diminished by the EPC transplantation. The EPC transplantation ameliorated the VILI. The mechanism may be primarily through the improvement of epithelial permeability, inhibition of local and systemic inflammation, and reduction in apoptosis.https://doi.org/10.1177/0963689719874048 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ying-nan Ju Ying-jie Geng Xue-ting Wang Jing Gong Jingli Zhu Wei Gao |
spellingShingle |
Ying-nan Ju Ying-jie Geng Xue-ting Wang Jing Gong Jingli Zhu Wei Gao Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation Cell Transplantation |
author_facet |
Ying-nan Ju Ying-jie Geng Xue-ting Wang Jing Gong Jingli Zhu Wei Gao |
author_sort |
Ying-nan Ju |
title |
Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation |
title_short |
Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation |
title_full |
Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation |
title_fullStr |
Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation |
title_full_unstemmed |
Endothelial Progenitor Cells Attenuate Ventilator-Induced Lung Injury with Large-Volume Ventilation |
title_sort |
endothelial progenitor cells attenuate ventilator-induced lung injury with large-volume ventilation |
publisher |
SAGE Publishing |
series |
Cell Transplantation |
issn |
0963-6897 1555-3892 |
publishDate |
2019-12-01 |
description |
Ventilator-induced lung injury (VILI) is a common complication that results from treatment with mechanical ventilation (MV) in acute respiratory distress syndrome (ARDS) patients. The present study investigated the effect of endothelial progenitor cell (EPC) transplantation on VILI. Wistar rats were divided into three groups ( n = 8): sham (S), VILI model (V) induced by tidal volume ventilation (17 mL/kg), and VILI plus EPC transplantation (VE) groups. The lung PaO 2 /FiO 2 ratio, pulmonary wet-to-dry (W/D) weight ratio, number of neutrophils, total protein, neutrophil elastase level, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and serum were examined. Furthermore, the histological and apoptotic analysis, and lung tissue protein expression analysis of Bax, Bcl-2, cleaved caspase-3, matrix metalloproteinase (MMP)-9, total nuclear factor kappa B (total-NF-κB), phosphorylated NF-κB (phospho-NF-κB) and myosin light chain (MLC) were performed. The ventilation-induced decrease in PaO 2 /FiO 2 ratio, and the increase in W/D ratio and total protein concentration were prevented by the EPC transplantation. The EPC transplantation (VE group) significantly attenuated the VILI-induced increased expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-8, MMP-9, phospho-NF-κB and MLC, neutrophil elastase levels and neutrophil counts in BALF. In addition, the anti-inflammatory factor IL-10 increased in the VE group. Furthermore, pulmonary histological injury and apoptosis (TUNEL-positive cells, increase in Bax and cleaved caspase-3) were considerably diminished by the EPC transplantation. The EPC transplantation ameliorated the VILI. The mechanism may be primarily through the improvement of epithelial permeability, inhibition of local and systemic inflammation, and reduction in apoptosis. |
url |
https://doi.org/10.1177/0963689719874048 |
work_keys_str_mv |
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