Angiotensin II receptors in human preadipocytes: Role in cell cycle regulation

Angiotensin II receptors in human preadipocytes: Role in cell cycle regulation
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DOI:
10.1210/en.140.1.154
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发表时间:
1999-01-01
期刊:
影响因子:
4.8
通讯作者:
Kral, JG
Kral, JG
中科院分区:
医学2区
文献类型:
--
作者:
Crandall, DL;Armellino, DC;Kral, JG

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被引文献

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血管紧张素II(AII)在人脂肪组织原代培养中对人前脂肪细胞生理学的作用进行了研究。受体结合研究表明,人前脂肪细胞表达高亲和力的AT亚型AII结合位点,因为I-125标记的[Sar(1),Ile(8)]AII结合迅速、饱和和特异。由于ALL先前已被证明影响肾上腺和心脏细胞的细胞周期,因此在人类前脂肪细胞中研究了ALII对周期进程的调节作用。AII刺激前脂肪细胞导致细胞周期的G(1)期进展,正如现在的细胞分析所确定的那样。所有的处理都与诱导细胞周期调节蛋白细胞周期蛋白D1的信使RNA表达有关,并呈剂量依赖关系。在AII刺激前用亚型选择性AT受体配体对细胞进行预处理,表明细胞周期蛋白的反应是通过AT受体介导的。在特定的分化介质中培养,通过流式细胞仪观察瘦素信息的表达和甘油三酯的积累,验证了细胞是前脂肪细胞的身份。这些发现表明,ALL对人类前脂肪细胞的细胞周期进程具有早期的受体介导的影响,这可能有助于向脂肪细胞表型分化。
The role of angiotensin II (AII) in human preadipocyte physiology has been investigated in primary cultures from human adipose tissue. Receptor binding studies indicated that human preadipocytes express a high affinity AII binding site of the AT, subtype, as binding of I-125-labeled [Sar(1),Ile(8)]AII was rapid, saturable, and specific. As All has previously been demonstrated to affect the cell cycle in adrenal and cardiac cells, the effect of AII on regulation of cycle progression was examined in human preadipocytes. Stimulation of preadipocytes with AII resulted in G(1) phase progression of the cell cycle, as determined by now cytometric analysis. AII treatment was associated with induction of expression of the messenger RNA for the cell cycle regulatory protein cyclin D1 in a dose-dependent manner. Pretreatment of cells with subtype-selective AT receptor ligands before AII stimulation indicated that the cyclin response was mediated via the AT, receptor. The identity of the cells as preadipocyte was verified by culture in a defined differentiation medium, observing both leptin message expression and triglyceride accumulation by flow cytometry. These findings indicate that All has early, receptor-mediated effects on cell cycle progression in human preadipocytes that may contribute to differentiation to the adipocyte phenotype.