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首页> 外文期刊>Cellular Signalling >Beneficial effects of PTP1B deficiency on brown adipocyte differentiation and protection against apoptosis induced by pro- and anti-inflammatory stimuli
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Beneficial effects of PTP1B deficiency on brown adipocyte differentiation and protection against apoptosis induced by pro- and anti-inflammatory stimuli

机译：PTP1B缺乏对促炎性和抗炎性刺激诱导的褐色脂肪细胞分化和防止凋亡的有益作用

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摘要

Insulin is an inducer of brown fat adipogenesis through the activation of a signalling network that involves positiveegative modulators. Given the importance of brown adipose tissue (BAT) for basal thermogenic energy expenditure, we investigated the role of PTP1B in the acquisition of terminal differentiated phenotype and in the apoptotic responses of brown adipocytes. Immortalized brown preadipocytes lacking (PTP1B(-/-)) or expressing (PTP1B(+/+)) PTP1B have been generated. PTP1B deficiency accelerated a full program of brown adipogenesis including induction of transcription factors, coactivators, adipogenic markers and signalling molecules. Fully differentiated PTP1B(-/-) brown adipocytes were resistant to tumor necrosis factor (TNF alpha)-induced apoptosis as these cells were protected against caspase-8 activation, FLIP degradation, Bid cleavage and caspase-3 activation compared to wild-type controls. These events were recovered by PTP1B rescue. Survival signalling including phosphorylation of IRS-1 and Akt/PKB and BcIxL expression were decreased in TNF alpha-treated PTP1B(-/-) cells but not in the wild-type. Similarly, PTP1B(-/-) brown adipocytes were protected against resveratrol-induced apoptosis. Phosphorylation of Akt/PKB and Foxo1 phosphorylation/acetylation decreased exclusively in resveratrol-treated wild-type cells, leading to nuclear localization of Foxo1 and up-regulation of Bim. Thus, PTP1B inhibition could be of benefit against obesity by counteracting TNF alpha-induced brown fat atrophy, and combined with resveratrol might improve low-grade inflammation.
机译：胰岛素通过激活涉及正/负调节剂的信号网络来诱导褐色脂肪的脂肪形成。考虑到棕色脂肪组织（BAT）对于基础生热能量消耗的重要性，我们研究了PTP1B在获得最终分化表型和棕色脂肪细胞凋亡反应中的作用。缺少（PTP1B（-/-））或表达（PTP1B（+ / +））PTP1B的永生化棕色前脂肪细胞已生成。 PTP1B缺乏促进了褐色脂肪形成的完整程序，包括诱导转录因子，共激活因子，脂肪形成标记和信号分子。与野生型对照相比，完全分化的PTP1B（-/-）棕色脂肪细胞对肿瘤坏死因子（TNF alpha）诱导的凋亡具有抵抗力，因为这些细胞可防止caspase-8激活，FLIP降解，Bid裂解和caspase-3激活。 。这些事件已通过PTP1B救援得以恢复。 TNF I处理的PTP1B（-/-）细胞中包括IRS-1和Akt / PKB磷酸化的存活信号和BcIxL表达降低，而野生型则没有。同样，PTP1B（-/-）棕色脂肪细胞被保护免受白藜芦醇诱导的细胞凋亡。仅在白藜芦醇处理过的野生型细胞中，Akt / PKB的磷酸化和Foxo1的磷酸化/乙酰化降低，导致Foxo1的核定位和Bim的上调。因此，PTP1B抑制作用可以通过抵抗TNFα诱导的褐色脂肪萎缩而有益于肥胖症，并且与白藜芦醇合用可能会改善低度炎症。

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