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血小板衍生生长因子依赖性细胞凋亡抑制在3T3-L1前脂肪细胞分化中的作用

The role of PDGF-dependent suppression of apoptosis in differentiating 3T3-L1 preadipocytes.

作者信息

Staiger H, Löffler G

机构信息

Institute for Biochemistry, Genetics and Microbiology, University of Regensburg, Germany.

出版信息

Eur J Cell Biol. 1998 Nov;77(3):220-7. doi: 10.1016/S0171-9335(98)80110-6.

Abstract

In a chemically defined serum-free culture system, platelet-derived growth factor (PDGF) as the only externally applied growth factor, in concert with corticosterone, 3-isobutyl-1-methylxanthine (IBMX) and low insulin (1nM), stimulates adipose conversion of 3T3-L1 preadipocytes. Omission of PDGF during the induction period results in loss of differentiation competence and apoptotic cell death. Induction of apoptosis is shown to be clearly mediated by PDGF withdrawal, since neither corticosterone nor IBMX affect the apoptotic behaviour of 3T3-L1 cells. Cell viability in the absence of the survival factor PDGF could be achieved by application of high insulin (1 microM) or ectopical expression of the anti-apoptotic proto-oncogene Bcl-2. However, PDGF-independent suppression of cell death does not trigger adipose conversion in the presence of corticosterone and IBMX. Therefore, we conclude that suppression of apoptosis per se is not permissive for differentiation of 3T3-L1 preadipocytes and PDGF might exert some additional differentiation-promoting effect(s).

摘要

在一个化学成分明确的无血清培养系统中,血小板衍生生长因子(PDGF)作为唯一外部添加的生长因子,与皮质酮、3 - 异丁基 - 1 - 甲基黄嘌呤(IBMX)和低浓度胰岛素(1nM)协同作用,刺激3T3 - L1前脂肪细胞向脂肪细胞转化。在诱导期去除PDGF会导致分化能力丧失和细胞凋亡死亡。由于皮质酮和IBMX均不影响3T3 - L1细胞的凋亡行为,因此细胞凋亡的诱导显然是由PDGF去除介导的。通过应用高浓度胰岛素(1μM)或抗凋亡原癌基因Bcl - 2的异位表达,可以在缺乏存活因子PDGF的情况下实现细胞存活。然而,在存在皮质酮和IBMX的情况下,不依赖PDGF的细胞死亡抑制并不会触发脂肪细胞转化。因此,我们得出结论,细胞凋亡的抑制本身并不允许3T3 - L1前脂肪细胞分化,并且PDGF可能发挥一些额外的促进分化的作用。

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