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首页> 外文期刊>Journal of cellular biochemistry. >Glycogen synthase kinase-3beta suppresses tumor necrosis factor-alpha expression in cardiomyocytes during lipopolysaccharide stimulation.
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Glycogen synthase kinase-3beta suppresses tumor necrosis factor-alpha expression in cardiomyocytes during lipopolysaccharide stimulation.

机译：糖原合酶激酶3β抑制脂多糖刺激过程中心肌细胞中的肿瘤坏死因子-α表达。

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摘要

This study was to investigate the role of glycogen synthase kinase-3beta (GSK-3beta) in cardiomyocyte tumor necrosis factor-alpha (TNF-alpha) expression induced by lipopolysaccharide (LPS). In cultured neonatal mouse cardiomyocytes, LPS induced TNF-alpha expression and increased GSK-3beta activation. Inhibition of GSK-3beta by SB216763 or by over-expression of a dominant negative mutant of GSK-3beta significantly enhanced TNF-alpha expression in LPS-stimulated cardiomyocytes, in association with an increase in p65 phosphorylation. In contrast, over-expression of GSK-3beta by adenoviral vectors containing wild-type GSK-3beta or a constitutively active GSK-3beta attenuated TNF-alpha expression induced by LPS. Further evidence to support the inhibitory role of GSK-3beta in TNF-alpha expression is that protein kinase B (Akt) signaling, an upstream inhibitor of GSK-3beta, promotes TNF-alpha expression in LPS-stimulated cardiomyocytes and this action of Akt signaling can be mimicked by GSK-3beta inactivation. Our study demonstrates that GSK-3beta plays an inhibitory role in cardiomyocyte TNF-alpha expression during LPS stimulation, and it may be a potential therapeutic target for sepsis.
机译：这项研究旨在调查糖原合酶激酶3β（GSK-3beta）在脂多糖（LPS）诱导的心肌细胞肿瘤坏死因子-α（TNF-α）表达中的作用。在培养的新生小鼠心肌细胞中，LPS诱导TNF-α表达并增加GSK-3beta活化。 SB216763或GSK-3beta显性负突变体的过表达抑制GSK-3beta会显着增强LPS刺激的心肌细胞中TNF-alpha的表达，并伴有p65磷酸化的增加。相反，含有野生型GSK-3beta或组成型活性GSK-3beta的腺病毒载体过表达GSK-3beta会减弱LPS诱导的TNF-α表达。支持GSK-3beta在TNF-alpha表达中的抑制作用的进一步证据是，蛋白激酶B（Akt）信号传导（GSK-3beta的上游抑制剂）促进LPS刺激的心肌细胞中TNF-alpha的表达以及Akt信号传导的这种作用。可以被GSK-3beta失活模拟。我们的研究表明，在LPS刺激过程中，GSK-3beta在心肌细胞TNF-α表达中起抑制作用，并且它可能是脓毒症的潜在治疗靶标。

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