Abstract
Gestational diabetes mellitus (GDM) is associated with an increased risk of adverse pregnancy outcomes. Increasing evidence shows that placentation defects may play important roles in GDM. However, our understanding of the human placenta remains limited. In this study, we generated a comprehensive transcriptomic profile of cellular signatures and transcriptomes in the human placenta in GDM using single-cell RNA sequencing (scRNA-seq), constructed a comprehensive cell atlas, and identified cell subtypes and subtype-specific marker genes. In addition, we investigated the placental cellular function and intercellular interactions in GDM. These findings help to elucidate the molecular mechanisms of GDM, and may facilitate the development of new approaches to GDM treatment and prevention.
Highlights
Gestational diabetes mellitus (GDM) increases the risk of adverse pregnancy outcomes, such as preterm birth, premature rupture of membranes, macrosomia and fetal distress
Some studies have shown that GDM-associated defects in Insulin resistance (IR) were tissue-type-dependent, and that glucose tolerance and insulin tolerance were impaired in GDM placenta [1]
We obtained a total of 27,220 cells from placental samples (14,591 from GDM samples and 12,629 from control samples)
Summary
Gestational diabetes mellitus (GDM) increases the risk of adverse pregnancy outcomes, such as preterm birth, premature rupture of membranes, macrosomia and fetal distress. Insulin resistance (IR) is considered as the central to the development of GDM. The precise mechanisms for the occurrence and development of GDM remain to be elucidated. The placenta is an important organ for material exchange between the fetus and mother, which is crucial to maintain a healthy pregnancy. Some studies have shown that GDM-associated defects in IR were tissue-type-dependent, and that glucose tolerance and insulin tolerance were impaired in GDM placenta [1]. Increasing evidence suggested that placental defects might play the important roles in GDM [2], related mainly to fatty acid placental transfer [3], specific hormones (placental lactogen, prolactin, oestradiol, etc.), and factors in the placental microenvironment, including cytokines [4], proteins, genes, miRNAs [5], lncRNAs [6], circRNAs [7]. At present, our understanding of the placenta remains very limited
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