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α-聚赖氨酸在 3T3-L1 前脂肪细胞中作为一种成脂诱导剂发挥作用。

α-Poly-L-lysine functions as an adipogenic inducer in 3T3-L1 preadipocytes.

机构信息

Marine Biotechnology Research Center, Korea Institute of Ocean Science and Technology, 385 Haeyang-ro, Busan, 49111, Republic of Korea.

Department of Ocean Science, Korea University of Science and Technology, Daejeon, 34113, Republic of Korea.

出版信息

Amino Acids. 2021 Apr;53(4):587-596. doi: 10.1007/s00726-020-02932-2. Epub 2021 Mar 20.

Abstract

α-Poly-L-lysine (PLL) has been used for various purposes such as cell attachment, immunization, and molecular delivery, and is known to be cytotoxic to several cell lines. Here, we studied the effect of PLL on the adipogenesis of 3T3-L1 cells and investigated the underlying mechanism. Differentiation media containing PLL with a molecular weight (MW) greater than 4 kDa enhanced lipid droplet formation and increased adipogenic marker levels, indicating an increase in adipocyte differentiation. PLL with a molecular weight between 30 and 70 kDa was more effective than PLL of other sizes in 3T3-L1 cell differentiation. Moreover, PLL induced 3T3-L1 adipogenesis in insulin-free adipocyte differentiation medium. Incubation with insulin and PLL exhibited greater adipogenesis than insulin treatment only even at a high concentration. PLL stimulated insulin signaling and augmented the signaling pathway when it was added with insulin. While PLL did not activate the glucocorticoid receptor, which is phosphorylated by dexamethasone (DEX), it showed a positive effect on the cAMP signal pathway when preadipocytes were treated with PLL and 3-isobutyl-1-methylxanthine (IBMX). Consistent with these results, incubation with PLL and DEX without IBMX induced adipocyte differentiation. We also observed that the mitotic clonal expansion phase was the critical stage in adipogenesis for inducing the effects of PLL. These results suggest that PLL functions as an adipogenic inducer in 3T3-L1 preadipocytes and PLL has a direct effect on insulin signaling, one of the main regulatory pathways.

摘要

α-聚-L-赖氨酸(PLL)已被用于各种用途,如细胞附着、免疫和分子递药,并且已知对几种细胞系具有细胞毒性。在这里,我们研究了 PLL 对 3T3-L1 细胞脂肪生成的影响,并探讨了其潜在机制。含有大于 4 kDa 分子量(MW)的 PLL 的分化培养基增强了脂滴的形成并增加了脂肪生成标志物的水平,表明脂肪细胞分化增加。分子量在 30 到 70 kDa 之间的 PLL 在 3T3-L1 细胞分化中比其他大小的 PLL 更有效。此外,PLL 在无胰岛素的脂肪细胞分化培养基中诱导 3T3-L1 脂肪生成。与仅用胰岛素处理相比,胰岛素和 PLL 孵育表现出更高的脂肪生成作用,即使在高浓度下也是如此。PLL 刺激胰岛素信号转导,并在与胰岛素一起添加时增强信号通路。虽然 PLL 不会激活被地塞米松(DEX)磷酸化的糖皮质激素受体,但当前脂肪细胞用 PLL 和 3-异丁基-1-甲基黄嘌呤(IBMX)处理时,它显示出对 cAMP 信号通路的积极影响。与这些结果一致,在没有 IBMX 的情况下用 PLL 和 DEX 孵育诱导脂肪细胞分化。我们还观察到,有丝分裂克隆扩张阶段是诱导 PLL 作用的脂肪生成的关键阶段。这些结果表明,PLL 在 3T3-L1 前脂肪细胞中作为脂肪生成诱导剂发挥作用,并且 PLL 对胰岛素信号转导具有直接影响,胰岛素信号转导是主要调节途径之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9998/8107076/c1a693988e4b/726_2020_2932_Fig1_HTML.jpg

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