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首页> 外文期刊>International Journal of Molecular Sciences >14-3-3γ Regulates Lipopolysaccharide-Induced Inflammatory Responses and Lactation in Dairy Cow Mammary Epithelial Cells by Inhibiting NF-κB and MAPKs and Up-Regulating mTOR Signaling
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14-3-3γ Regulates Lipopolysaccharide-Induced Inflammatory Responses and Lactation in Dairy Cow Mammary Epithelial Cells by Inhibiting NF-κB and MAPKs and Up-Regulating mTOR Signaling

机译：14-3-3γ通过抑制NF-κB和MAPKs并上调mTOR信号传导来调节脂多糖诱导的奶牛乳腺上皮细胞的炎症反应和泌乳

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As a protective factor for lipopolysaccharide (LPS)-induced injury, 14-3-3γ has been the subject of recent research. Nevertheless, whether 14-3-3γ can regulate lactation in dairy cow mammary epithelial cells (DCMECs) induced by LPS remains unknown. Here, the anti-inflammatory effect and lactation regulating ability of 14-3-3γ in LPS-induced DCMECs are investigated for the first time, and the molecular mechanisms responsible for their effects are explored. The results of qRT-PCR showed that 14-3-3γ overexpression significantly inhibited the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and inducible nitric oxide synthase (iNOS). Enzyme-linked immunosorbent assay (ELISA) analysis revealed that 14-3-3γ overexpression also suppressed the production of TNF-α and IL-6 in cell culture supernatants. Meanwhile, CASY-TT Analyser System showed that 14-3-3γ overexpression clearly increased the viability and proliferation of cells. The results of kit methods and western blot analysis showed that 14-3-3γ overexpression promoted the secretion of triglycerides and lactose and the synthesis of β-casein. Furthermore, the expression of genes relevant to nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPKs) and lactation-associated proteins were assessed by western blot, and the results suggested that 14-3-3γ overexpression inactivated the NF-κB and MAPK signaling pathways by down-regulating extracellular signal regulated protein kinase (ERK), p38 mitogen-activated protein kinase (p38MAPK) and inhibitor of NF-κB (IκB) phosphorylation levels, as well as by inhibiting NF-κB translocation. Meanwhile, 14-3-3γ overexpression enhanced the expression levels of β-casein, mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase 1 (S6K1), serine/threonine protein kinase Akt 1 (AKT1), sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activated receptor gamma (PPARγ). These results suggest that 14-3-3γ was able to attenuate the LPS-induced inflammatory responses and promote proliferation and lactation in LPS-induced DCMECs by inhibiting the activation of the NF-κB and MAPK signaling pathways and up-regulating mTOR signaling pathways to protect against LPS-induced injury.
机译：作为脂多糖（LPS）诱导的损伤的保护因子，14-3-3γ已成为近期研究的主题。然而，由LPS诱导的14-3-3γ是否能调节奶牛乳腺上皮细胞（DCMEC）的泌乳尚不清楚。在这里，首次研究了14-3-3γ在LPS诱导的DCMEC中的抗炎作用和泌乳调节能力，并探讨了影响其作用的分子机制。 qRT-PCR结果表明，14-3-3γ过表达显着抑制肿瘤坏死因子-α（TNF-α），白细胞介素-6（IL-6），白细胞介素-1β（IL-1β）和诱导型mRNA的表达。一氧化氮合酶（iNOS）。酶联免疫吸附试验（ELISA）分析显示14-3-3γ过表达还抑制细胞培养上清液中TNF-α和IL-6的产生。同时，CASY-TT分析仪系统显示14-3-3γ过表达明显增加了细胞的活力和增殖。试剂盒方法和蛋白质印迹分析的结果表明，14-3-3γ的过表达促进了甘油三酸酯和乳糖的分泌以及β-酪蛋白的合成。此外，通过蛋白质印迹法评估了与核因子-κB（NF-κB）和有丝分裂原激活的蛋白激酶（MAPKs）和与泌乳相关的蛋白有关的基因的表达，结果表明14-3-3γ的高表达使蛋白的失活。通过下调细胞外信号调节蛋白激酶（ERK），p38促分裂原激活蛋白激酶（p38MAPK）和NF-κB抑制剂（IκB）磷酸化水平以及抑制NF-κB移位来调节NF-κB和MAPK信号通路。同时，14-3-3γ过表达增强了β-酪蛋白，哺乳动物雷帕霉素靶标（mTOR），核糖体蛋白S6激酶1（S6K1），丝氨酸/苏氨酸蛋白激酶Akt 1（AKT1），固醇调节元件结合蛋白的表达水平。 1（SREBP1）和过氧化物酶体增殖物激活受体γ（PPARγ）。这些结果表明，14-3-3γ能够通过抑制NF-κB和MAPK信号通路的激活以及上调mTOR信号通路来减弱LPS诱导的DCMECs的炎症反应，并促进LPS诱导的DCMEC的增殖和泌乳。保护免受LPS引起的伤害。

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