Obstetric and neonatal outcomes after frozen–thawed embryos transfer with laser-assisted hatching: a retrospective cohort study

Pan, Jiaping; Liang, Shan; Huang, Mei Yuan; Zhao, Ming; Kong, Peng Cheng; Liu, Yi Ping; Teng, Xiao Ming; Wu, Hai Xia

doi:10.1007/s00404-021-06153-0

Cited by 4 publications

(1 citation statement)

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“…It is also one of the predictors of long-term type 2 diabetes in pregnant women and their offspring [ 5 ]. Those with severe GDM or poor control of blood glucose may ultimately suffer from some adverse pregnancy outcomes, such as hypertension of pregnancy, premature delivery, stillbirth, fetal development and giant babies [ 30 ]. Therefore, reasonable control of the condition and blood glucose can greatly reduce the impact on the health of mothers and children.…”

Section: Discussionmentioning

confidence: 99%

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Zhang

Bai

2021

Bioengineered

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Multiple studies have confirmed that adipokines are compactly relevant to insulin resistance and participate in the pathogenesis of gestational diabetes mellitus (GDM). This paper aimed to study the effects of C1q/tumor necrosis factor related protein (CTRP)6 on the phenotypes of trophoblast cells, covering cell proliferation, invasion and migration, and initially explore the mechanism. High glucose was used to induce trophoblast cells to establish an in vitro model. The expression levels of CTRP6 were firstly determined, and then the effects of CTRP6 knockdown on cell viability, apoptosis, migration and invasion were assessed using CCK8, TUNEL, wound healing, Transwell assays. Moreover, the role of peroxisome proliferator-activated receptor gamma (PPARγ), probable target of CTRP6, was evaluated through co-transfection with PPARγ overexpression vector. The results of the present study revealed that CTRP6 and PPARγ were both upregulated in high glucose-induced cells. And CTRP6 knockdown could significantly elevate the abilities of cell viability, migration and invasion, and avoid cell apoptosis. In addition, PPARγ overexpression was found to restrain the protective effects of CTRP6 knockdown on the above aspects, indicating CTRP6 played a role in trophoblast cells via inhibiting PPARγ expression. In conclusion, CTRP6 regulated the viability, migration and invasion of high glucose-induced gestational trophoblast cells through PPARγ signaling.

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Section: Discussionmentioning

confidence: 99%