Abstract
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.
Highlights
Gestational diabetes mellitus (GDM) is frequently caused by abnormal glucose resistance or impairment during the gestational period, and mainly presents as elevated fasting blood glucose and insulin resistance, accompanied with inflammation, increased secretion of inflammatory factors and abnormal body immunity.[1,2] Gestational diabetes mellitus is a unique subtype of diabetes which occurs in pregnant women worldwide.[3]
Gestational diabetes mellitus placental tissues showed higher Long noncoding RNA (lncRNA) MALAT1 expression compared to a normal control group (p < 0.05)
Real-time PCR was used to measure the expression of lncRNA MALAT1 in GDM, which showed that it was significantly higher in placental tissues than in normal pregnant placentas (p < 0.05; Fig. 1)
Summary
Gestational diabetes mellitus (GDM) is frequently caused by abnormal glucose resistance or impairment during the gestational period, and mainly presents as elevated fasting blood glucose and insulin resistance, accompanied with inflammation, increased secretion of inflammatory factors and abnormal body immunity.[1,2] Gestational diabetes mellitus is a unique subtype of diabetes which occurs in pregnant women worldwide.[3]. Gestational diabetes mellitus (GDM) is frequently caused by abnormal glucose resistance or impairment during the gestational period, and mainly presents as elevated fasting blood glucose and insulin resistance, accompanied with inflammation, increased secretion of inflammatory factors and abnormal body immunity.[1,2]. Gestational diabetes mellitus patients have elevated glucose levels and glucose catabolic disorder, caused by insulin resistance and leading to cellular glucose metabolic disorder. GDM can cause placental abruption, gestational hypertension, premature delivery, or congenital abnormality, leading to severe and long-lasting threats to maternal/fetal health.[9,10]. Recent studies have found that long noncoding RNA (lncRNA) participates in the regulation of various cellular processes. Gestational diabetes mellitus (GDM) severely threatens maternal and fetal health. Long noncoding RNA (lncRNA) participates in the regulation of various cellular processes
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