IR@PKUHSC  > 北京大学第三临床医学院
学科主题临床医学
Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions
Guo, Weixin1; Li, Zhihong2; Xie, Xiaoyun3; Qin, Tiehe1; Wu, Yan1; Li, Zhou1; Chai, Jing4; Yi, Frank5; Tan, Tao5; Zhu, Hua5; Wang, Shouhong1
关键词Urinary Trypsin Inhibitor (UTI) Endothelial progenitor cells (EPCs) Acute lung injury (ALI) Akt/eNOS
刊名CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
2015
DOI10.1159/000430279
36期:3页:1059-1068
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Physiology
研究领域[WOS]Cell Biology ; Physiology
关键词[WOS]RESPIRATORY-DISTRESS-SYNDROME ; REPERFUSION INJURY ; VASCULAR REPAIR ; OLEIC-ACID ; LIPOPOLYSACCHARIDE ; PATHOGENESIS ; SURFACTANT ; PNEUMONIA ; PROTECTS ; PATHWAY
英文摘要

Background: Urinary Trypsin Inhibitor (UTI) is involved in various aspects of tissue repair, regeneration and development. However, the potential role of UTI in protection against acute lung injury (ALI) remains largely unknown. In the present study, we demonstrated that UTI treatment could ameliorate ALI induced by oleic acid (OA) treatment in rabbit model. Methods: Intravenous application of UTI (10000 U/kg/d) significantly improved the pathologies associated with OA-induced ALI. The lungs were stained with hematoxylin and eosin to scored the lung injury. Peripheral blood mononuclear cells were isolated by density gradient centrifugation with Ficoll-Plaque Plus. The proliferation and ability of tube structure formation of EPCs were observed and the level of phosphorylated Akt protein expression and eNOS protein expression were assayed. Results: Consistent with pathological scores, UTI treatment significantly reduced wet/dry ratio of OA injured lungs. A quantification of capillary density revealed that UTI treatment led to about 2 fold increase over uninjured control and about 1.5 fold increase over PBS treatment. The capacity for tube formation of EPCs on ECM gel was significantly reduced in the ALI group and recovered with UTI treatment. Quantification of western blot bands was summarized and showed that UTI treatment activates Akt/eNOS signaling. NO production could contribute to the improvement of EPCs function by UTI treatment. Conclusions: UTI-induced phosphorylation/activation of eNOS and Akt, increases the intracellular level of NO, thereby improving tube formation and proliferation function of EPCs. EPCs function is crucial for re-endothelialization after denuding injuries of arteries. Copyright (C) 2015 S. Karger AG, Basel

语种英语
WOS记录号WOS:000357833400021
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63605
专题北京大学第三临床医学院
作者单位1.Peking Univ, Hosp 3, Beijing 100871, Peoples R China
2.Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Geriatr Inst, Guangzhou 510100, Guangdong, Peoples R China
3.Chenzhou First Peoples Hosp, Div Gen Surg, Chenzhou, Hunan, Peoples R China
4.Zhejiang Univ, Coll Anim Sci, Hangzhou 310003, Zhejiang, Peoples R China
5.Ohio State Univ, Wexner Med Ctr, Davis Heart & Lung Res Inst, Dept Surg, Columbus, OH 43210 USA
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GB/T 7714
Guo, Weixin,Li, Zhihong,Xie, Xiaoyun,et al. Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions[J]. CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,2015,36(3):1059-1068.
APA Guo, Weixin.,Li, Zhihong.,Xie, Xiaoyun.,Qin, Tiehe.,Wu, Yan.,...&Wang, Shouhong.(2015).Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions.CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,36(3),1059-1068.
MLA Guo, Weixin,et al."Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions".CELLULAR PHYSIOLOGY AND BIOCHEMISTRY 36.3(2015):1059-1068.
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