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学科主题: 临床医学
题名:
Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions
作者: 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
发表日期: 2015
DOI: 10.1159/000430279
卷: 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
所属项目编号: 01201114
项目资助者: Techpool Fund ; National Key Clinical Specialties Construction Projects of China
WOS记录号: WOS:000357833400021
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63605
Appears in Collections:北京大学第三临床医学院_期刊论文

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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

Recommended Citation:
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.
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