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首页> 外文期刊>Journal of biochemical and molecular toxicology >Trichostatin A, an Inhibitor of Histone Deacetylase, Inhibits the Viability and Invasiveness of Hypoxic Rheumatoid Arthritis Fibroblast-Like Synoviocytes via PI3K/Akt Signaling
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Trichostatin A, an Inhibitor of Histone Deacetylase, Inhibits the Viability and Invasiveness of Hypoxic Rheumatoid Arthritis Fibroblast-Like Synoviocytes via PI3K/Akt Signaling

机译：Trichostatin A是组蛋白脱乙酰基酶的抑制剂，可通过PI3K / Akt信号传导抑制低氧类风湿关节炎成纤维细胞样滑膜细胞的活力和侵袭性

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摘要

This study was undertaken to explore the effects of trichostatin A (TSA), an inhibitor of histone deacetylase, on the viability, apoptosis, and invasiveness of hypoxic rheumatoid arthritis fibroblast-like synoviocytes (RA FLSs). RA FLSs were exposed to hypoxia for 24 h in the presence or absence of 2 M TSA and tested for cell viability, apoptosis, invasion, and gene expression. The involvement of the phosphatidylinositol-3-kinase (PI3K)/Akt pathway was checked. TSA significantly inhibited the viability and induced apoptosis of hypoxic RA FLSs, compared to vehicle control. TSA blocked hypoxia-induced invasion of RA FLSs during Matrigel invasion assays and reduced the expression of matrix metalloproteinases (MMP-2 and MMP-9) and PI3K and phosphorylation of Akt. Overexpression of constitutively active Akt reversed TSA-mediated suppression of invasiveness and downregulation of MMP-2 and MMP-9. Our results indicate the antisurvival and antiinvasive activities of TSA in hypoxic RA FLSs, which is associated with inactivation of PI3K/Akt signaling.
机译：进行这项研究以探讨组蛋白脱乙酰基酶抑制剂曲古抑菌素A（TSA）对低氧类风湿关节炎成纤维细胞样滑膜细胞（RA FLSs）的活力，凋亡和侵袭性的影响。在有或没有2 M TSA的情况下，将RA FLS暴露于缺氧环境下24小时，并测试其细胞活力，凋亡，侵袭和基因表达。检查了磷脂酰肌醇-3-激酶（PI3K）/ Akt途径的参与。与媒介物对照相比，TSA显着抑制了低氧RA FLS的活力并诱导了其凋亡。在基质胶侵袭试验中，TSA阻断了低氧诱导的RA FLS的侵袭，并降低了基质金属蛋白酶（MMP-2和MMP-9）和PI3K的表达以及Akt的磷酸化。组成型活性Akt的过表达逆转了TSA介导的对侵袭性的抑制以及MMP-2和MMP-9的下调。我们的结果表明，TSA在低氧性RA FLS中具有抗生存和抗侵袭活性，这与PI3K / Akt信号的失活有关。

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