中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2012年
9期
775-779
,共5页
杨海兵%严金川%苏红玲%袁伟%徐良洁
楊海兵%嚴金川%囌紅玲%袁偉%徐良潔
양해병%엄금천%소홍령%원위%서량길
动脉粥样硬化%抗原,CD137%活化T细胞核因子类
動脈粥樣硬化%抗原,CD137%活化T細胞覈因子類
동맥죽양경화%항원,CD137%활화T세포핵인자류
Atherosclerosis%Antigens,CD137%NFATC transcription factors
目的 探讨CD137-CD137配体(CD137L)相互作用对载脂蛋白E基因敲除(ApoE-/)小鼠活化T细胞核因子c1( NFATc1)表达的影响.方法 采用ApoE-/-小鼠颈动脉硅胶圈置入法快速建立动脉粥样斑块模型.分别采用免疫组织化学及流式细胞术检测小鼠颈动脉斑块及脾脏淋巴细胞中NFATc1表达.体外培养的小鼠淋巴细胞NFATc1 mRNA和蛋白表达分别应用RT-PCR和流式细胞技术检测.结果 体内抗CD137特异性刺激CD137-CD137L轴后,斑块及脾脏中淋巴细胞中NFATc1表达增加.体外培养的淋巴细胞中抗CD137刺激CD137-CD137L轴后,淋巴细胞NFATc1 mRNA和蛋白表达明显上调,刺激浓度以20 μg/ml时作用最强,刺激时间24 h最佳(P＜0.05).抗CD137L特异性阻断CD137-CD137L轴能明显抑制NFATc1 mRNA及蛋白表达,浓度以20 μg/ml时抑制作用最强,抑制时间24 h最佳(P＜0.05).结论 CD137-CD137L相互作用能调控ApoE-/-小鼠NFATc1的表达.
目的 探討CD137-CD137配體(CD137L)相互作用對載脂蛋白E基因敲除(ApoE-/)小鼠活化T細胞覈因子c1( NFATc1)錶達的影響.方法 採用ApoE-/-小鼠頸動脈硅膠圈置入法快速建立動脈粥樣斑塊模型.分彆採用免疫組織化學及流式細胞術檢測小鼠頸動脈斑塊及脾髒淋巴細胞中NFATc1錶達.體外培養的小鼠淋巴細胞NFATc1 mRNA和蛋白錶達分彆應用RT-PCR和流式細胞技術檢測.結果 體內抗CD137特異性刺激CD137-CD137L軸後,斑塊及脾髒中淋巴細胞中NFATc1錶達增加.體外培養的淋巴細胞中抗CD137刺激CD137-CD137L軸後,淋巴細胞NFATc1 mRNA和蛋白錶達明顯上調,刺激濃度以20 μg/ml時作用最彊,刺激時間24 h最佳(P＜0.05).抗CD137L特異性阻斷CD137-CD137L軸能明顯抑製NFATc1 mRNA及蛋白錶達,濃度以20 μg/ml時抑製作用最彊,抑製時間24 h最佳(P＜0.05).結論 CD137-CD137L相互作用能調控ApoE-/-小鼠NFATc1的錶達.
목적 탐토CD137-CD137배체(CD137L)상호작용대재지단백E기인고제(ApoE-/)소서활화T세포핵인자c1( NFATc1)표체적영향.방법 채용ApoE-/-소서경동맥규효권치입법쾌속건립동맥죽양반괴모형.분별채용면역조직화학급류식세포술검측소서경동맥반괴급비장림파세포중NFATc1표체.체외배양적소서림파세포NFATc1 mRNA화단백표체분별응용RT-PCR화류식세포기술검측.결과 체내항CD137특이성자격CD137-CD137L축후,반괴급비장중림파세포중NFATc1표체증가.체외배양적림파세포중항CD137자격CD137-CD137L축후,림파세포NFATc1 mRNA화단백표체명현상조,자격농도이20 μg/ml시작용최강,자격시간24 h최가(P＜0.05).항CD137L특이성조단CD137-CD137L축능명현억제NFATc1 mRNA급단백표체,농도이20 μg/ml시억제작용최강,억제시간24 h최가(P＜0.05).결론 CD137-CD137L상호작용능조공ApoE-/-소서NFATc1적표체.
Objective To investigate the effects of CD137-CD137L interaction on the nuclear factor of activated T cells c1 (NFATc1) in apolipoprotein E knockout (ApoE-/-) mice.Methods Atherosclerotic plaque model was produced by rapid perivascular carotid collar placement in ApoE-/- mice.In vivo,the expression of NFATc1 in mice plaque and lymphocytes was detected by immunohistochemical and flow cytometry, respectively.In vitro, the NFATc1 mRNA and protein expressions in cultured lymphocytes of ApoE -/- mice were measured by RT-PCR and flow cytometry,respectively.Results In vivo,after stimulating CD137-CD137L signal pathway, the expression of NFATc1 was significantly upregulated in the atherosclerotic plaques and lymphocytes.In vitro,the mRNA and protein expressions of NFATc1 in cultured leukocytes of ApoE-/- mice were also significantly increased,the maximal effect appeared post 20 μg/ml anti-CD137 mAb- stimulation and reached maximum at 24 h at any concentrations.Anti-CD137L mAb significantly downregulated the mRNA and protein expressions of NFATcl in lymphocytes of ApoE -/- mice,maximal effect appeared at 20 μg/ml anti-CD137L mAb and reached minimum at 24 h.Conclusion CD137-CD137L interactions can modulate the expression of NFATc1 in this ApoE -/- mice atherosclerotic plaque model.
