IR@PKUHSC  > 北京大学基础医学院
学科主题基础医学
The antifibrosis effect of adrenomedullin in human lung fibroblasts
Hao, Shu-Ling1; Yu, Zhong-He1; Qi, Bao-Shen2; Luo, Ji-Zheng1; Wang, Wei-Ping3
关键词Adrenomedullin Fibrosis Hypoxia Proliferation Tgf-beta 1
刊名EXPERIMENTAL LUNG RESEARCH
2011-12-01
DOI10.3109/01902148.2011.623823
37期:10页:615-626
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Respiratory System
资助者National Nature Science Foundation of China ; National Nature Science Foundation of China
研究领域[WOS]Respiratory System
关键词[WOS]ENDOTHELIAL GROWTH-FACTOR ; HUMAN DERMAL FIBROBLASTS ; PULMONARY-HYPERTENSION ; COLLAGEN-SYNTHESIS ; FACTOR-BETA ; HUMAN SKIN ; LIFE-SPAN ; HYPOXIA ; CELLS ; OXYGEN
英文摘要

Adrenomedullin (AM) is a regulatory peptide involved in cellular proliferation and protein synthesis. The authors investigated AM and the AM receptor system in the human fetal lung fibroblasts (HFLFs), and assessed whether AM can inhibit proliferation and collagen synthesis in HFLFs under hypoxia. Fibroblasts were exposed to hypoxia (2% O-2) after the addition of AM. The effects of AM and transforming growth factor beta 1 (TGF-beta 1) on the proliferation of fibroblasts were determined by the methanethiosulfonate (MTS) assay. Total collagen synthesis was determined by [H-3] proline incorporation. TGF-beta 1 levels in the culture supernatant were measured by enzyme-linked immunosorbent assay (ELISA). The concentration of intracellular calciumion ([Ca2+](i)) in fibroblasts was detected with a laser scanning confocal microscope. AM, adrenomedullin receptor (ADMR), calcitonin receptor-like receptor (CRLR), AM receptor chaperone receptor activity-modifying protein-1 (RAMP1), RAMP2, and RAMP3 were detected in the HFLFs. The hypoxia-induced increases in cell proliferation, collagen synthesis, and TGF-beta 1 production were inhibited by AM. AM also inhibited proliferation and collagen synthesis in fibroblasts induced by TGF-beta 1. AM caused a decrease of the hypoxia-induced [Ca2+](i) in fibroblasts. This study suggests that AM is produced by HFLFs and AM may function as an antifibrosis factor that protects cells from hypoxic pulmonary damage through its receptors.

语种英语
所属项目编号30070336
资助者National Nature Science Foundation of China ; National Nature Science Foundation of China
WOS记录号WOS:000297057600005
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54717
Collection北京大学基础医学院
作者单位1.Beijing PLA, Mil Gen Hosp, Dept Resp Dis, Beijing, Peoples R China
2.Chinese Acad Med Sci, Inst Basic Med Sci, Dept Physiol & Pathophysiol, Peking Union Med Coll, Beijing 100730, Peoples R China
3.Peking Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Beijing 100871, Peoples R China
Recommended Citation
GB/T 7714
Hao, Shu-Ling,Yu, Zhong-He,Qi, Bao-Shen,et al. The antifibrosis effect of adrenomedullin in human lung fibroblasts[J]. EXPERIMENTAL LUNG RESEARCH,2011,37(10):615-626.
APA Hao, Shu-Ling,Yu, Zhong-He,Qi, Bao-Shen,Luo, Ji-Zheng,&Wang, Wei-Ping.(2011).The antifibrosis effect of adrenomedullin in human lung fibroblasts.EXPERIMENTAL LUNG RESEARCH,37(10),615-626.
MLA Hao, Shu-Ling,et al."The antifibrosis effect of adrenomedullin in human lung fibroblasts".EXPERIMENTAL LUNG RESEARCH 37.10(2011):615-626.
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