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作 者:杨海兵[1] 严金川[1] 苏红玲[1] 袁伟[1] 徐良洁[1]
出 处:《中华心血管病杂志》2012年第9期775-779,共5页Chinese Journal of Cardiology
基 金:国家自然科学基金(81170279);江苏省自然科学基金(BK2011486);江苏省科教兴卫工程(LJ201116);镇江市社会发展项目(SH2010012);镇江市心血管病重点实验室($$2012001)
摘 要:目的 探讨CDl37-CDl37配体(CDl37L)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(NFATcl)表达的影响。方法采用ApoE^-/-小鼠颈动脉硅胶圈置人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NFATcl表达。体外培养的小鼠淋巴细胞NFATclmRNA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CDl37特异性刺激CDl37.CDl37L轴后,斑块及脾脏中淋巴细胞中NFATcl表达增加。体外培养的淋巴细胞中抗CDl37刺激CDl37-CDl37L轴后,淋巴细胞NFATclmRNA和蛋白表达明显上调,刺激浓度以20μg/m1时作用最强,刺激时间24h最佳(P〈0.05)。抗CDl37L特异性阻断CDl37-CDl37L轴能明显抑制NFATclmRNA及蛋白表达,浓度以20μg/ml时抑制作用最强,抑制时间24h最佳(P〈0.05)。结论CDl37-CDl37L相互作用能调控ApoE。-小鼠NFATcl的表达。Objective To investigate the effects of CD137-CD137L interaction on the nuclear factor of activated T ceils cl (NFATcl) 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 NFATcl in mice plaque and lymphocytes was detected by immunohistochemical and flow cytometry, respectively. In vitro, the NFATcl 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 NFATcl was significantly upregulated in the atherosclerotic plaques and lymphocytes. In vitro, the mRNA and protein expressions of NFATcl 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 NFATcl in this ApoE^-/- mice atherosclerotic plaque model.
关 键 词:动脉粥样硬化 抗原 CDl37 活化T细胞核因子类
分 类 号:R543.5[医药卫生—心血管疾病]
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