Nuclear-enriched abundant transcript 1 (NEAT1), a vital long noncoding RNA (lncRNA), exhibits the functions in disparate cancers. Nevertheless, the influences of NEAT1 in congenital heart disease (CHD) remain unreported. The research delves into whether NEAT1 affects H9c2 cells apoptosis and autophagy under the hypoxia condition. Overexpressed NEAT1 vector was transfected into H9c2 cells; then, functions of NEAT1 in cell viability, apoptosis, autophagy, PI3K/AKT/mTOR and JAK1/STAT3 pathways were detected in H9c2 cells under hypoxia condition. Expression of NEAT1 and miR-181b in hypoxia and blood samples from CHD was evaluated. After miR-181b inhibitor transfection, functions of miR-181b repression in the above-mentioned cell behavior and PI3K/AKT/mTOR and JAK1/STAT3 pathways were reassessed. Overexpressed NEAT1 clearly allayed hypoxia-triggered H9c2 cells apoptosis and autophagy. The decreased NEAT1 and miR-181b were showcased in hypoxia and blood samples from CHD; meanwhile, elevated miR-181b evoked by overexpressed NEAT1 was observed in hypoxia-managed H9c2 cells. More importantly, miR-181b inhibition obviously overturned the influences of NEAT1 in hypoxia-affected H9c2 cells apoptosis and autophagy. Besides, overexpressed NEAT1 facilitated PI3K/AKT/mTOR and JAK1/STAT3 activations via enhancing miR-181b. The research exposed that NEAT1 eased hypoxia-triggered H9c2 cells apoptosis and autophagy by expediting PI3K/AKT/mTOR and JAK1/STAT3 pathways via elevating miR-181b.

中文翻译：

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LncRNA富含核的丰富转录物1通过介导microRNA-181b调节缺氧引起的细胞凋亡和自噬。

核富集的丰富转录本1（NEAT1）是至关重要的长非编码RNA（lncRNA），在不同的癌症中表现出功能。尽管如此，NEAT1对先天性心脏病（CHD）的影响仍未报道。该研究探讨了NEAT1在缺氧条件下是否影响H9c2细胞的凋亡和自噬。将过表达的NEAT1载体转染到H9c2细胞中；然后，在缺氧条件下，在H9c2细胞中检测了NEAT1在细胞活力，凋亡，自噬，PI3K / AKT / mTOR和JAK1 / STAT3途径中的功能。评估了CHD缺氧和血液样本中NEAT1和miR-181b的表达。在miR-181b抑制剂转染后，重新评估了miR-181b阻抑在上述细胞行为以及PI3K / AKT / mTOR和JAK1 / STAT3途径中的功能。过度表达的NEAT1明显缓解了低氧触发的H9c2细胞的凋亡和自噬。NEAT1和miR-181b的减少在冠心病的低氧和血液样本中显示。同时，在低氧处理的H9c2细胞中观察到过表达的NEAT1引起的miR-181b升高。更重要的是，miR-181b的抑制作用显然会破坏NEAT1对缺氧影响的H9c2细胞凋亡和自噬的影响。此外，过表达的NEAT1通过增强miR-181b促进了PI3K / AKT / mTOR和JAK1 / STAT3的激活。该研究表明，NEAT1通过提高miR-181b的速度来加快PI3K / AKT / mTOR和JAK1 / STAT3通路，从而缓解了低氧触发的H9c2细胞的凋亡和自噬。在缺氧处理的H9c2细胞中观察到过表达的NEAT1引起的miR-181b升高。更重要的是，miR-181b的抑制作用显然会破坏NEAT1对缺氧影响的H9c2细胞凋亡和自噬的影响。此外，过表达的NEAT1通过增强miR-181b促进了PI3K / AKT / mTOR和JAK1 / STAT3的激活。该研究表明，NEAT1通过提高miR-181b的速度来加快PI3K / AKT / mTOR和JAK1 / STAT3通路，从而缓解了低氧触发的H9c2细胞的凋亡和自噬。在缺氧处理的H9c2细胞中观察到过表达的NEAT1引起的miR-181b升高。更重要的是，miR-181b的抑制作用显然会破坏NEAT1对缺氧影响的H9c2细胞凋亡和自噬的影响。此外，过表达的NEAT1通过增强miR-181b促进了PI3K / AKT / mTOR和JAK1 / STAT3的激活。该研究表明，NEAT1通过提高miR-181b的速度来加快PI3K / AKT / mTOR和JAK1 / STAT3通路，从而缓解了低氧触发的H9c2细胞的凋亡和自噬。