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首页> 外文期刊>Biochemical and Biophysical Research Communications >Human umbilical cord-derived mesenchymal stem cells protect from hyperoxic lung injury by ameliorating aberrant elastin remodeling in the lung of O 2 -exposed newborn rat
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Human umbilical cord-derived mesenchymal stem cells protect from hyperoxic lung injury by ameliorating aberrant elastin remodeling in the lung of O 2 -exposed newborn rat

机译：人脐带衍生的间充质干细胞通过改善异常的Elastin重塑在O 2的肺中的异常弹性蛋白重新损伤免受高氧肺损伤

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摘要

Abstract The incidence and mortality rates of bronchopulmonary dysplasia (BPD) remain very high. Therefore, novel therapies are imminently needed to improve the outcome of this disease. Human umbilical cord-derived mesenchymal stem cells (UC-MSCs) show promising therapeutic effects on oxygen-induced model of BPD. In our experiment, UC-MSCs were intratracheally delivered into the newborn rats exposed to hyperoxia, a well-established BPD model. This study demonstrated that UC-MSCs reduce elastin expression stimulated by 90% O 2 in human lung fibroblasts-a (HLF-a), and inhibit HLF-a transdifferentiation into myofibroblasts. In addition, the therapeutic effects of UC-MSCs in neonatal rats with BPD, UC-MSCs could inhibit lung elastase activity and reduce aberrant elastin expression and deposition in the lung of BPD rats. Overall, this study suggested that UC-MSCs could ameliorate aberrant elastin expression in the lung of hyperoxia-induced BPD model which may be associated with suppressing increased TGFβ1 activation. Highlights ? UC-MSCs inhibit elastin expression in the human lung fibroblasts. ? UC-MSCs inhibit elastase activity in the lung of BPD rats. ? UC-MSCs could rescue berrant elastin expression and deposition in the lung of BPD rats.
机译：摘要支气管扩张发育不良（BPD）的发病率和死亡率仍然非常高。因此，需要新的疗法来改善这种疾病的结果。人的脐带衍生的间充质干细胞（UC-MSCs）表明对BPD的氧诱导的模型有前途的治疗效果。在我们的实验中，UC-MSCs含有肿瘤内递送到暴露于高氧的新生大鼠中，是一个完善的BPD模型。该研究表明，UC-MSCs将ELASTIN表达减少在人肺成纤维细胞-A（HLF-A）中90％O 2刺激，并抑制HLF-A转染到肌纤维细胞中。此外，UC-MSCs在具有BPD的新生大鼠中的治疗效果，UC-MSCs可以抑制肺弹性蛋白酶活性并减少BPD大鼠肺中的异常弹性蛋白表达和沉积。总体而言，本研究表明，UC-MSCs可以在高氧诱导的BPD模型的肺中改善异常的弹性蛋白表达，这可能与抑制增加的TGFβ1活化。强调 ？ UC-MSCs抑制人肺成纤维细胞中的弹性蛋白表达。还UC-MSCs在BPD大鼠的肺中抑制弹性蛋白酶活性。还UC-MSCs可以在BPD大鼠肺中拯救BERRANT ELASTIN表达和沉积。

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  • 来源
  • 作者

    Chen Hou; Danyi Peng; Li Gao; Daiyin Tian; Jihong Dai; Zhengxiu Luo; Enmei Liu; Hong Chen; Lin Zou; Zhou Fu;

  • 作者单位

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

    Pediatrics Research Institute Children's Hospital of Chongqing Medical University Ministry of;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    Bronchopulmonary dysplasia; UC-MSCs; Elastin; α-SMA; TGF-β1;

    机译：Bronchoplermonarary dysplasia;UC-MSCs;弹性蛋白;α-SMA;TGF-β1;

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