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The Contribution of LTB4/BLT1 Axis to the Progression of Sys...

The Contribution of LTB4/BLT1 Axis to the Progression of Systemic Sclerosis by Regulating Myofibroblast Formation

作     者:Liang Minrui Jiaoyan lv Zhixing Jiang Yinluo Xiong Rui He Hejian Zou 

作者单位:Division of RheumatologyHuashan Hospital Institute of RheumatologyImmunology and AllergyFudan University Department of ImmunologySchool of Basic Medical SciencesFudan University Biotherapy Research CenterFudan University 

会议名称:《第十一届全国免疫学学术大会》

会议日期:2016年

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

关 键 词:Leukotriene B4(LTB4) BLT1 systemic sclerosis(SSc) interstitial lung disease(ILD) 

摘      要:Leukotriene B4(LTB4),a lipid mediator of inflammation,plays a key role in the autoimmune and inflammatory diseases via its high affinity receptor *** is recognized to be critical in the progression of systemic sclerosis(SSc),but the mechanism is still *** aimed to use BLT1-/-mice and BLT1 specific inhibitor to reveal the contribution of LTB4/BLT1 axis to the progression of SSc in a modified SSc-interstitial lung disease(ILD) mouse model by delivering bleomycin(BLM) via an osmotic *** the present study,LTB4 was observed to be up-regulated in the plasma of SSc ***,immunohistochemical analysis demonstrated overexpressions of BLT1 and leukotriene A4 hydrolase(LTA4H),the biosynthetic enzyme for LTB4,in both skin and lung tissues of SSc-ILD *** addition,the levels of BLT1 and LTB4 H were also increasedin the skin and lung tissues of SSc-ILD ***1-/-mice did not manifest the phenotype of SSc following the BLM treatment in the SSc-ILD mouse *** the reduction of α-SMA+ myofibroblasts was also found in the skin and lung tissues of BLT1-/-mice following the administration of BLM,compared with those in wide type ***,the addition of LTB4 was observed to promote fibroblast-myofibroblast transition and endothelial-myofibroblast transition in vitro using primary cell culture,which were reversed by BLT1 *** addition,LTB4 induced phosphorylation of Akt and m TOR in a time dependent manner in fibroblast,also fibroblast-myofibroblast transition induced by LTB4 was blocked by Akt or m TOR ***,LTB4 was not shown to stimulate the release of TGF-β1 in fibroblast,and TGF-β receptor antagonist was not shown to inhibit fibroblast-myofibroblast *** results uncover a possible role for LTB4/BLT1 driven myofibroblast formation in SSc-ILD pathogenesis and identify a pathway that may be amenable to therapeutic targeting.

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