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Up-Regulation of miR-130b-3p Activates the PTEN/PI3K/AKT/NF-κB Pathway to Defense against Mycoplasma gallisepticum (HS Strain) Infection of Chicken

机译:miR-130b-3p的上调激活PTEN / PI3K / AKT / NF-κB途径以防止鸡的支原体脑蛋白(HS菌株)感染

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摘要

Mycoplasma gallisepticum (MG) is the pathogen of chronic respiratory disease (CRD), hallmarked by vigorous inflammation in chickens, causing the poultry industry enormous losses. miRNAs have emerged as important regulators of animal diseases. Previous miRNA sequencing data has demonstrated that miR-130b-3p is up-regulated in MG-infected chicken embryo lungs. Therefore, we aimed to investigate the function of miR-130b-3p in MG infection of chickens. RT-qPCR results confirmed that miR-130b-3p was up-regulated both in MG-infected chicken embryo lungs and chicken embryonic fibroblast cells (DF-1 cells). Furthermore, functional studies showed that overexpression of miR-130b-3p promoted MG-infected DF-1 cell proliferation and cell cycle, whereas inhibition of miR-130b-3p weakened these cellular processes. Luciferase reporter assay combined with gene expression data supported that phosphatase and tensin homolog deleted on chromosome ten (PTEN) was a direct target of miR-130b-3p. Additionally, overexpression of miR-130b-3p resulted in up-regulations of phosphatidylinositol-3 kinase (PI3K), serine/threonine kinase (AKT), and nuclear factor-κB (NF-κB), whereas inhibition of miR-130b-3p led to the opposite results. Altogether, upon MG infection, up-regulation of miR-130b-3p activates the PI3K/AKT/NF-κB pathway, facilitates cell proliferation and cell cycle via down-regulating PTEN. This study helps to understand the mechanism of host response to MG infection.
机译:支原体Gallisepticum(Mg)是慢性呼吸道疾病(CRD)的病原体,通过鸡中剧烈炎症的标记,导致家禽行业巨大的损失。 MiRNA已成为动物疾病的重要调节因素。先前的miRNA测序数据已经证明MIR-130B-3P在MG感染的鸡胚肺中上调。因此,我们旨在探讨MIR-130B-3P在鸡Mg感染中的功能。 RT-QPCR结果证实,MIR-130B-3P在MG感染的鸡胚肺和鸡胚成纤维细胞(DF-1细胞)中上调。此外,功能性研究表明,miR-130b-3p的过度表达促进了Mg感染的DF-1细胞增殖和细胞周期,而MiR-130b-3p的抑制削弱了这些细胞过程。 Luciferase报道器测定结合基因表达数据,支持磷酸酶和染色体10(PTEN)上缺失的磷酸酶和Tensin同源物是MiR-130B-3P的直接靶标。另外,miR-130b-3p的过表达导致磷脂酰肌醇-3激酶(pi3k),丝氨酸/苏氨酸激酶(akt)和核因子-κb(nf-κB)的um-curemitaitupt。抑制miR-130b-3p导致了相反的结果。在Mg感染后,MIR-130B-3P的上调激活PI3K / AKT / NF-κB途径,通过降压PTEN促进细胞增殖和细胞周期。本研究有助于了解宿主对Mg感染的机制。

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