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谷氨酰胺合成酶通过提高细胞内谷氨酰胺水平,使分化的脂肪细胞对促炎刺激产生脱敏作用。

Glutamine synthetase desensitizes differentiated adipocytes to proinflammatory stimuli by raising intracellular glutamine levels.

作者信息

Palmieri Erika Mariana, Spera Iolanda, Menga Alessio, Infantino Vittoria, Iacobazzi Vito, Castegna Alessandra

机构信息

Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.

Department of Science, University of Basilicata, Potenza, Italy.

出版信息

FEBS Lett. 2014 Dec 20;588(24):4807-14. doi: 10.1016/j.febslet.2014.11.015. Epub 2014 Nov 20.

DOI:10.1016/j.febslet.2014.11.015
PMID:25451225
Abstract

The role of glutamine synthetase (GS) during adipocyte differentiation is unclear. Here, we assess the impact of GS on the adipocytic response to a proinflammatory challenge at different differentiation stages. GS expression at the late stages of differentiation desensitized mature adipocytes to bacterial lipopolysaccharide (LPS) by increasing intracellular glutamine levels. Furthermore, LPS-activated mature adipocytes were unable to produce inflammatory mediators; LPS sensitivity was rescued following GS inhibition and the associated drop in intracellular glutamine levels. The ability of adipocytes to differentially respond to LPS during differentiation negatively correlates to GS expression and intracellular glutamine levels. Hence, modulation of intracellular glutamine levels by GS expression represents an endogenous mechanism through which mature adipocytes control the inflammatory response.

摘要

谷氨酰胺合成酶(GS)在脂肪细胞分化过程中的作用尚不清楚。在此,我们评估了GS在不同分化阶段对脂肪细胞促炎刺激反应的影响。分化后期的GS表达通过提高细胞内谷氨酰胺水平,使成熟脂肪细胞对细菌脂多糖(LPS)脱敏。此外,LPS激活的成熟脂肪细胞无法产生炎症介质;GS抑制以及细胞内谷氨酰胺水平随之下降后,LPS敏感性得以恢复。脂肪细胞在分化过程中对LPS的不同反应能力与GS表达和细胞内谷氨酰胺水平呈负相关。因此,通过GS表达调节细胞内谷氨酰胺水平是成熟脂肪细胞控制炎症反应的一种内源性机制。

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