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学科主题: 临床医学
题名:
Regulation of lung fibroblast activation by annexin A1
作者: Jia, Yuan1,2; Morand, Eric F.1; Song, Wuqi1,3; Cheng, Qiang1; Stewart, Alastair4; Yang, Yuan H.1
刊名: JOURNAL OF CELLULAR PHYSIOLOGY
发表日期: 2013-02-01
DOI: 10.1002/jcp.24156
卷: 228, 期:2, 页:476-484
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]: INDUCED LEUCINE-ZIPPER ; FORMYL PEPTIDE RECEPTORS ; LIPOXIN A(4) RECEPTOR ; RHEUMATOID-ARTHRITIS ; UP-REGULATION ; GLUCOCORTICOID ACTIONS ; PULMONARY-FIBROSIS ; PROTEIN-KINASES ; GENE-EXPRESSION ; CELL-LINE
英文摘要:

Annexin-A1 (AnxA1) is a glucocorticoid-induced protein with multiple actions in the regulation of inflammatory cell activation. The contribution of AnxA1 to human cell biology is not well understood. We investigated the contribution of AnxA1 and its receptor, formyl-peptide receptor 2 (FPR2), to the regulation of inflammatory responses in human normal lung fibroblasts (NLF). Silencing constitutive AnxA1 expression in NLF using small interfering RNA (siRNA) was associated with moderate but significant increases in tumor necrosis factor (TNF)-induced proliferation and interleukin (IL)-6 production, accompanied by reduction of ERK and NF-kappa B activity. AnxA1 regulation of ERK and NF-kappa B activation was associated with effects on proliferation. Blocking FPR2 using the specific antagonist WRW4 mimicked the effects of AnxA1 silencing on TNF-induced proliferation, IL-6, ERK, and NF-kappa B activation. AnxA1 silencing also impaired inhibitory effects of glucocorticoid on IL-6 production and on the expression of glucocorticoid-induced leucine zipper (GILZ), but blocking FPR2 failed to mimic these effects of AnxA1 silencing. These data suggest that AnxA1 regulates TNF-induced proliferation and inflammatory responses in lung fibroblasts, via effects on the ERK and NF-kappa B pathways, which depend on FPR2. AnxA1 also mediates effects of glucocorticoids and GILZ expression, but these effects appear independent of FPR2. These findings suggest that mimicking AnxA1 actions might have therapeutic potential in chronic inflammatory lung diseases. J. Cell. Physiol. 228: 476484, 2013. (C) 2012 Wiley Periodicals, Inc.

语种: 英语
所属项目编号: ID436692
项目资助者: Australian National Health and Medical Research Council
WOS记录号: WOS:000310486200026
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/68227
Appears in Collections:北京大学第二临床医学院_期刊论文

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作者单位: 1.Monash Univ, Ctr Inflammatory Dis, So Clin Sch, Fac Med Nursing & Hlth Sci,Monash Med Ctr, Clayton, Vic 3168, Australia
2.Peking Univ, Peoples Hosp, Dept Rheumatol & Immunol, Beijing 100871, Peoples R China
3.Harbin Med Univ, Heilongjiang Key Lab Immun & Infect, Dept Microbiol, Harbin, Peoples R China
4.Univ Melbourne, Dept Pharmacol, Parkville, Vic 3052, Australia

Recommended Citation:
Jia, Yuan,Morand, Eric F.,Song, Wuqi,et al. Regulation of lung fibroblast activation by annexin A1[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2013,228(2):476-484.
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