Department of Obstetrics, Yantai Yuhuangding Hospital, China.
Adv Clin Exp Med. 2020 Aug;29(8):903-910. doi: 10.17219/acem/121524.
Gestational diabetes mellitus (GDM) severely threatens maternal and fetal health. Long non-coding RNA (lncRNA) participates in the regulation of various cellular processes.
Previous studies have identified the role of lncRNA MALAT1 in diabetic retinopathy-related inflammation. However, the role of lncRNA MALAT1 in GDM has not been reported yet.
Real-time polymerase chain reaction (RT-PCR) was used to measure the lncRNA MALAT1 expression level in placental tissues from GDM patients and from a normal pregnant group. Placental trophoblastic-derived cell line HTR8 cells were divided into a control group, an siRNA negative control group and a MALAT1 siRNA group. The cells underwent RT-PCR analysis of lncRNA MALAT1 expression, an MTT assay of cell proliferation, and a transwell assay of cell invasion and migration. In addition, enzyme-linked immunosorbent assay (ELISA) was used to analyze the level of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6). Western blotting was used to measure the changes of the tumor growth factor β (TGF-β)/nuclear factor-kappa B (NF-κB) signaling pathway.
Gestational diabetes mellitus placental tissues showed higher lncRNA MALAT1 expression compared to a normal control group (p < 0.05). After siRNA intervention, lncRNA MALAT1 showed decreased expression in the trophoblastic layer; inhibited trophoblastic cell proliferation, migration, or invasion; decreased the secretion of inflammatory factors TNF-α and IL-6; and suppressed the expression of TGF-β and NF-κB compared to that of the control and siRNA-NC groups (p < 0.05).
Gestational diabetes mellitus appears to upregulate lncRNA MALAT1. Downregulation of lncRNA MALAT1 inhibits inflammation and suppresses the proliferation, invasion and migration of GDM placental trophoblastic cells, possibly by modulating the TGF-β/NF-κB signaling pathway.
妊娠期糖尿病（GDM）严重威胁母婴健康。长链非编码 RNA（lncRNA）参与多种细胞过程的调节。
先前的研究已经确定了 lncRNA MALAT1 在糖尿病性视网膜病变相关炎症中的作用。然而，lncRNA MALAT1 在 GDM 中的作用尚未报道。
实时聚合酶链反应（RT-PCR）用于测量 GDM 患者和正常妊娠组胎盘组织中 lncRNA MALAT1 的表达水平。胎盘滋养层衍生细胞系 HTR8 细胞分为对照组、siRNA 阴性对照组和 MALAT1 siRNA 组。对细胞进行 lncRNA MALAT1 表达的 RT-PCR 分析、细胞增殖的 MTT 分析以及细胞侵袭和迁移的 Transwell 分析。此外，还使用酶联免疫吸附试验（ELISA）分析肿瘤坏死因子-α（TNF-α）和白细胞介素 6（IL-6）的水平。使用 Western blot 测定转化生长因子-β（TGF-β）/核因子-κB（NF-κB）信号通路的变化。
与正常对照组相比，GDM 胎盘组织中 lncRNA MALAT1 的表达更高（p < 0.05）。经过 siRNA 干预后，滋养层层中的 lncRNA MALAT1 表达降低；抑制滋养层细胞的增殖、迁移或侵袭；降低炎症因子 TNF-α和 IL-6 的分泌；与对照组和 siRNA-NC 组相比，抑制 TGF-β和 NF-κB 的表达（p < 0.05）。
GDM 似乎上调了 lncRNA MALAT1。下调 lncRNA MALAT1 抑制了 GDM 胎盘滋养层细胞的炎症，并抑制了其增殖、侵袭和迁移，可能通过调节 TGF-β/NF-κB 信号通路。
