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首页> 外文期刊>Journal of Cellular Physiology >Decoupled syndecan 1 mRNA and protein expression is differentially regulated by angiotensin II in macrophages.
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Decoupled syndecan 1 mRNA and protein expression is differentially regulated by angiotensin II in macrophages.

机译：解耦syndecan 1 mRNA和蛋白表达受不同血管紧张素ⅱ在吗巨噬细胞。

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It has been established that syndecan-1 is an important modulator of events relevant to acute tissue repair and chronic injury responses. The current studies were designed to examine syndecan-1 expression during atherosclerotic lesion formation and whether angiotensin II influences syndecan-1 expression in macrophages. ApoE knockout mice maintained on an atherogenic diet were treated for 8 weeks with an infusion of angiotensin II to induce atherosclerosis. Immunohistochemistry was employed to characterize the expression of syndecan-1 in atherosclerotic lesions. Quantitative real-time PCR (QRTPCR) was used to define the role of angiotensin II and responsible signaling pathways involved syndecan-1 expression in RAW264.7 murine macrophages. Protein expression and shedding were characterized by fluorescence activated cell sorting (FACS) and slot blot analysis. Syndecan-1 was abundantly expressed in macrophages located within early atherosclerotic lesions. Accordingly, we hypothesized that angiotensin II regulates syndecan-1 expression in macrophages. A time- and dose-dependent study was performed in RAW264.7 macrophages. QRTPCR demonstrated maximum syndecan-1 mRNA up-regulation at 6 h after 500 nM AgII stimulation (threefold; P < 0.05). Through administration of specific inhibitors, we established that ERK/MAPK, PI3K and JNK signaling pathways mediated this effect. FACS and slot blot analyses demonstrated that cAMP induced posttranscriptional syndecan-1 protein expression in a dose-dependent manner with or without initial angiotensin II stimulation. In particular, angiotensin II induced an increase in cell surface syndecan-1 (mean fluorescence intensity: 147 +/- 5.7 vs. 176 +/- 4.8; P < 0.05; n = 3) and accelerated syndecan-1 shedding. Angiotensin II is a potent regulator of syndecan-1 expression in atherosclerotic lesions via a specific effect on macrophages that is mediated by ERK/MAPK, PI3K, and JNK signaling pathways.
机译：它已经建立,syndecan-1是一个重要的事件相关的急性调制器组织修复和慢性损伤反应。目前的研究是为了检查syndecan-1表达在动脉粥样硬化病变形成和血管紧张素ⅱ影响syndecan-1巨噬细胞中表达。载脂蛋白e基因敲除小鼠保持动脉饮食与注入治疗8周血管紧张素ⅱ诱导动脉粥样硬化。免疫组织化学是用来描述syndecan-1的表达在动脉粥样硬化病变。血管紧张素ⅱ和用于定义的角色负责相关信号通路syndecan-1 RAW264.7小鼠表达巨噬细胞。荧光激活细胞的特征排序(流式细胞仪)和槽污点分析。在巨噬细胞大量表达位于在早期动脉粥样硬化病变。因此,我们推测,血管紧张素ⅱ调节syndecan-1巨噬细胞中表达。在执行时间和剂量依赖性研究RAW264.7巨噬细胞。syndecan-1 mRNA上调后6 h 500海里AgII刺激(3倍;管理特定抑制剂,我们证实ERK / MAPK PI3K和物信号通路介导这一效应。分析表明,诱导转录后的syndecan-1蛋白表达剂量依赖性的方式有或没有最初的血管紧张素ⅱ的刺激。血管紧张素ⅱ诱导的增加细胞表面syndecan-1(平均荧光强度:147 + / - 5.7 vs 176 + / - 4.8;n = 3)和加速syndecan-1脱落。血管紧张素ⅱ是一个强有力的监管机构syndecan-1表达在动脉粥样硬化病变巨噬细胞通过一个特定的影响由ERK / MAPK、PI3K和物的信号通路。

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