Literature DB >> 30391008

Endothelial progenitor cells attenuate the lung ischemia/reperfusion injury following lung transplantation via the endothelial nitric oxide synthase pathway.

Wei Gao1, Tao Jiang1, Yan-Hong Liu1, Wen-Gang Ding1, Chang-Chun Guo1, Xiao-Guang Cui2.   

Abstract

OBJECTIVE: Endothelial progenitor cells (EPCs) can improve endothelial integrity. This study aimed to examine the effects and the mechanism of EPCs on lung ischemia-reperfusion injury (LIRI).
METHODS: Wistar rats were randomized into the sham or the left lung transplantation group. The recipients were randomized and treated with vehicle as the LIRI group, with EPC as the EPC group, or with N5-(1-iminoethyl)-l-ornithine-pretreated EPC as the EPC/L group (n = 8 per group). The ratios of arterial oxygen partial pressure to fractional inspiratory oxygen were measured. The lung wet-to-dry weight ratios, protein levels, and injury, as well as the levels of plasma cytokines, were examined. The levels of endothelin (ET)-1, endothelial nitric oxide synthase (eNOS), phosphorylated eNOS, inducible NOS, phosphorylated myosin light chain, nuclear factor-κBp65, Bax, Bcl-2, cleaved caspase-3, and myeloperoxidase in the graft lungs were detected.
RESULTS: Compared with the LIRI group, EPC treatment significantly increased the ratios of arterial oxygen partial pressure to fractional inspiratory oxygen and decreased the lung wet-to-dry weight ratios and protein levels in the grafts, accompanied by increasing eNOS expression and phosphorylation, but decreasing endothelin-1, inducible NOS, phosphorylated nuclear factor-kBp65, phosphorylated myosin light chain expression, and myeloperoxidase activity. EPCs reduced lung tissue damage and apoptosis associated with decreased levels of Bax and cleaved caspase-3 expression, but increased Bcl-2 expression. EPC treatment significantly reduced the levels of serum proinflammatory factors, but elevated levels of interleukin-10. In contrast, the protective effect of EPCs were mitigated and abrogated by N5-(1-iminoethyl)-l-ornithine pretreatment.
CONCLUSIONS: Data indicated that EPC ameliorated LIRI by increasing eNOS expression.
Copyright © 2018 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  endothelial progenitor cells; inflammation; ischemia/reperfusion injury; lung transplantation

Year:  2018        PMID: 30391008     DOI: 10.1016/j.jtcvs.2018.08.092

Source DB:  PubMed          Journal:  J Thorac Cardiovasc Surg        ISSN: 0022-5223            Impact factor:   5.209


  10 in total

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10.  Lipoxin A4 attenuates the lung ischaemia reperfusion injury in rats after lung transplantation.

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  10 in total

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