Endothelial Colony-forming Cells Attenuate Ventilator-induced Lung Injury in Rats with Acute Respiratory Distress Syndrome

Ju, Yingnan; Gong, Jianping; Wang, Xueting; Zhu, Jingli

doi:10.1016/j.arcmed.2018.08.006

Cited by 8 publications

(21 citation statements)

References 43 publications

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“…We isolated and cultured ECFCs from Sprague-Dawley rats according to a previous study [14]. First, we collected peripheral blood and isolated mononuclear cells using density-gradient centrifugation with Ficoll-Plaque Plus (Amersham Pharmacia Biotech, Uppsala, Sweden).…”

Section: Isolation Of Ecfcsmentioning

confidence: 99%

“…The cells were identified according to the results of our previous study [14]. Approximately 4 ×10 4 cells/well were incubated with fluorescein isothiocyanate (FITC)-conjugated Ulex europaeus agglutinin-1 (50 μg/ml) (UEA-1, Sigma-Aldrich, Saint Louis, USA) and DiI-acetyl-low-density lipoprotein (LDL) (30 μg/ml) (Invitrogen, Carlsbad, USA).…”

Section: Characterization Of Ecfcsmentioning

confidence: 99%

“…Briefly, the pathology indexes included alveolar congestion, lung oedema, haemorrhage, infiltration of neutrophils into the airspace/vessel wall and alveolar wall thickness [14]. The scoring was as follows:…”

Section: Histopathologic Injury Evaluationmentioning

confidence: 99%

“…As the outgrowth of endothelial progenitor cells, endothelial colony-forming cells (ECFCs) have high proliferative potency [7] and anti-inflammatory effects [8]. ECFCs reduced ischaemic injury and ventilator-induced lung injury via their high proliferative capacity and anti-inflammatory effects [9,10] [11]. Considering the key role of inflammation in lung injury induced by CPB, we hypothesized that ECFCs can ameliorate lung injury after CPB.…”

Section: Introductionmentioning

confidence: 99%

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Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Sun

Zhao

Tai

et al. 2020

Preprint

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Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pretreated ECFCs. After 24 hours of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight, was evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score: 1.62±0.51 vs 5.37±0.91 vs 3.37±0.89 vs 4.37±0.74; PaO 2 /FiO 2 : 389±12 vs 233±36 vs 338±28 vs 287±30; wet/dry weight: 3.11±0.32 vs 6.71±0.73 vs 4.66±0.55 vs 5.52±0.57; protein levels: 134±22 vs 442±99 vs 225±41 vs 337±53, all P<0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2 . Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

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Section: Isolation Of Ecfcsmentioning

confidence: 99%

Section: Characterization Of Ecfcsmentioning

confidence: 99%

Section: Histopathologic Injury Evaluationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Sun

Zhao

Tai

et al. 2020

Preprint

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“…Under an inflammatory process, ventilation can damage endothelium that express high levels of ET-1 and promote MLC phosphorylation [30]. ET-1 can enhance the iNOS expression, which not only produces reactive oxidative species (ROS), but also promotes inflammatory cytokine production [31] [32].…”

Section: Ac2-26 Protects Against Lps-induced Apoptosis In Human Alveomentioning

confidence: 99%

Annexin A1 peptide Ac2-26 mitigates ventilator-induced lung injury in acute respiratory distress syndrome rats by enhancing endothelial nitric oxide synthase activity

Zhao

Zhang

et al. 2020

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Background Mechanical ventilation is an important therapeutic strategy for supporting patients with acute respiratory distress syndrome (ARDS). However, ventilation can exacerbate lung injury and lead to ventilator-induced lung injury (VILI). This study aimed to evalaute the effect and mechanism of Annexin A1 (AnexA1) peptide Ac2-26 on VILI in ARDS rats. Methods To evalaute the effect and mechanism of Annexin A1 (AnexA1) peptide Ac2-26 on VILI in ARDS rats, Male SD rats were anesthetized, and intubated, followed by injected with vehicle as the control S group or with lipopolysaccharides (LPS) to induce ARDS. The ARD rats were ventilated, randomized and injected intravenously with vehicle, Ac2-26 or Ac2-26 and L-NIO (an inhibitor of nitric oxide synthase) as the V, VA and VA/L groups, respectively. Their arterial blood gases were analyzed longitudinally for PaO 2 /FiO 2 ratio, and the wet-to-dry lung weights and total protein concentrations in bronchoalveolar lavage fluid (BALF) were measured. The lung injury and inflammatory factors were quantified. The oxidative stress response was measured. The impact of Ac2-26 on the LPS-related cytotoxicity against A549 cells was analyzed. Results Compared with the S group, ARDS and ventilation impaired the lung function and caused lung injury in rats. Compared with V group, Ac2-26 treatment significantly ameliorated the lung function, reduced the VILI-related alveolocapillary permeability, lung injury and endothelial/epithelial cell apoptosis, oxidative stress and inflammation in VILI rats, but promoted AKT1 expression and eNOS phosphorylation, which were partially inhibited by co-treatment with L-NIO. Moreover, Ac2-26 protected against LPS-induced apoptosis of human A549 cells in vitro . Conclusions Ac2-26 effectively mitigated the severity of VILI partially by enhancing endothelial nitric oxide synthase expression in the lung of rats.

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Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability

Liu

Feng

et al. 2019

Inflammation

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Endothelial Colony-forming Cells Attenuate Ventilator-induced Lung Injury in Rats with Acute Respiratory Distress Syndrome

Cited by 8 publications

References 43 publications

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Annexin A1 peptide Ac2-26 mitigates ventilator-induced lung injury in acute respiratory distress syndrome rats by enhancing endothelial nitric oxide synthase activity

Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability

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