Regulation of Placental Angiogenesis

Chen, Dong‐bao; Zheng, Jing

doi:10.1111/micc.12093

Cited by 175 publications

(123 citation statements)

References 139 publications

Supporting

Mentioning

118

Contrasting

Unclassified

Order By: Relevance

“…Insulin resistance in peripheral tissues in women with GDM is exacerbated, but few studies have examined the extent of insulin resistance in placenta in this disease and the ways in which this resistance could contribute to alter the placental transport of nutrients [18,19]. Moreover, insulin, along with glucose, is involved in the regulation of angiogenesis and vasculogenesis in the fetus [20,21], where they bind to fetal endothelial cells [22]. Thus, fetal hyperinsulinemia may also contribute to the hypervascular placenta typical of GDM [23].…”

Section: Functions Of Insulin Within the Placentamentioning

confidence: 99%

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Ruiz-Palacios

Ruiz–Alcaraz²,

Sánchez-Campillo³

et al. 2017

Ann Nutr Metab

View full text Add to dashboard Cite

Background: Gestational diabetes mellitus (GDM) is associated with increased fetal adiposity, which may increase the risk of obesity in adulthood. The placenta has insulin receptors and maternal insulin can activate its signaling pathways, affecting the transport of nutrients to the fetus. However, the effects of diet or insulin treatment on the placental pathophysiology of GDM are unknown. Summary: There are very few studies on possible defects in the insulin signaling pathway in the GDM placenta. Such defects could influence the placental transport of nutrients to the fetus. In this review we discuss the state of insulin signaling pathways in placentas of women with GDM, as well as the role of exogenous insulin in placental nutrient transport to the fetus, and fetal adiposity. Key Messages: Maternal insulin in the third trimester is correlated with fetal abdominal circumference at that time, suggesting the important role of insulin in this process. Since treatment with insulin at the end of pregnancy may activate placental nutrient transport to the fetus and promote placental fatty acid transfer, it would be interesting to improve maternal hyperlipidemia control in GDM subjects treated with this hormone. More research in this area with high number of subjects is necessary.

show abstract

Section: Functions Of Insulin Within the Placentamentioning

confidence: 99%

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Ruiz-Palacios

Ruiz–Alcaraz²,

Sánchez-Campillo³

et al. 2017

Ann Nutr Metab

View full text Add to dashboard Cite

show abstract

“…This process is necessary for the development of the fetal vascular system in the placental villous tree and development of an adequate uteroplacental circulation. 5 Soluble fms-like tyrosine kinase (sFlt-1), an antiangiogenic factor secreted by endothelial cells, can block the effect of PlGF. 4 Previous studies showed that lower PlGF levels can disrupt the normal process of neoangiogenesis, whereas higher sFlt-1 levels during pregnancy can lead to systemic endothelial dysfunction.…”

mentioning

confidence: 99%

Influence of Maternal Angiogenic Factors During Pregnancy on Microvascular Structure in School-Age Children

et al. 2015

View full text Add to dashboard Cite

Reduced placental growth factor (PlGF) levels and higher soluble fms-like tyrosine kinase (sFlt-1) levels in mothers during pregnancy may have persistent effects on vascular structures in their offspring. We examined whether angiogenic factors during pregnancy also affect childhood retinal microvasculature in a population-based prospective cohort study among 3505 mothers and their children. We measured maternal PlGF and sFlt-1 in the first and second trimester of pregnancy. At the age of 6, we measured childhood retinal arteriolar and venular calibers from digitized retinal photographs. We performed multiple linear regression models, taking maternal and childhood sociodemographic and lifestyle-related characteristics, birth characteristics, and childhood current body mass index and blood pressure into account. We observed that first trimester maternal PlGF and sFlt-1 levels were not associated with childhood retinal arteriolar caliber. Lower second trimester maternal PlGF levels, but not sFlt-1 levels, were associated with narrower childhood retinal arteriolar caliber (difference: −0.09 SD score [95% confidence interval, −0.16 to 0.01], per SD score decrease in PlGF). This association was not explained by maternal and childhood sociodemographic and lifestyle-related characteristics, birth characteristics, or childhood current body mass index and blood pressure. Maternal PlGF and sFlt-1 levels in the first or second trimester were not associated with childhood retinal venular caliber. Our results suggest that lower maternal second trimester PlGF levels affect the microvascular development in the offspring, leading to narrower retinal arteriolar caliber in childhood. Further studies are needed to confirm these findings and to explore the underlying mechanisms and long-term cardiovascular consequences.

show abstract

“…31,32 Our results evidenced that TiO 2 NP treatment resulted in placental vascular collapse and it impaired the formation of an intricate network of fetal vessels. Similar to our results, Yamashita et al found that spiral artery canals failed to form and blood flow was significantly reduced in the fetal vascular sinuses of 70 nm TiO 2 NP-treated mice.…”

mentioning

confidence: 83%

“…32 Furthermore, Stapleton et al reported that thrombosis was observed in the pulmonary vascular system of TiO 2 NP-treated mice, which could be induced by the blocking of blood vessels with TiO 2 particles. 33 In addition, uNK cells are short-lived, terminally differentiated and the most abundant lymphocyte in the uterus, and play a vital role in vascularization, spiral arteriole modification and placentation.…”

mentioning

confidence: 99%

Gestational exposure to titanium dioxide nanoparticles impairs the placentation through dysregulation of vascularization, proliferation and apoptosis in mice

Zhang

Xie

Zhou

et al. 2018

IJN

View full text Add to dashboard Cite

Background Titanium dioxide nanoparticles (TiO 2 NPs) have recently found applications in a wide variety of consumer goods. TiO 2 NPs exposure significantly increases fetal deformities and mortality. However, the potential toxicity of TiO 2 NPs on the growth and development of placenta has been rarely studied during mice pregnancy. Purpose The objective of this study was to investigate the effects of maternal exposure of TiO 2 NPs on the placentation. Methods Mice were administered TiO 2 NPs by gavage at 0, 1 and 10 mg/kg/day from gestational day (GD) 1 to GD 13. Uteri and placentas from these mice were collected and counted the numbers of implanted and resorbed embryo and measured the placental weight on GD 13. Placental morphometry was observed by hematoxylin and eosin staining. The levels of Hand1, Esx1 , Eomes , Hand2 , Ascl2 and Fra1 mRNA were assessed by qRT-PCR. Uterine NK (uNK) cells were detected by using DBA lectin. Laminin immunohistochemical staining was to identify fetal vessels. Western blotting and transmission electron micrograph (TEM) were used to assess the apoptosis of placenta. Results No treatment-related difference was observed in the numbers of implanted and resorbed embryos and weight of placenta between the groups. However, 1 mg/kg/day TiO 2 NPs treatment significantly reduced the ratio of placenta/body weight on GD 13. The proportion of spongiotrophoblast in the 10 mg/kg/day dose group became higher than that in the control group, yet that of labyrinth was significantly lower in 10 mg/kg/day mice. The expression levels of Hand1 , Esx1 , Eomes , Hand2 , Ascl2 and Fra1 mRNA markedly decreased in TiO 2 NP treated placentas. Furthermore, TiO 2 NPs treatment impaired the formation of intricate networks of fetal vessels and reduced the number of uNK cells, and inhibited proliferation and induced apoptosis of placenta by nuclear pyknosis, the activation of caspase-3 and upregulation of Bax protein and downregulation of Bcl-2 protein on GD 13. Conclusion Gestational exposure to TiO 2 NPs significantly impairs the growth and development of placenta in mice, with a mechanism that seems to be involved in the dysregulation of vascularization, proliferation and apoptosis. Therefore, our results suggested the need for great caution while handling of the nanomaterials by workers and specially pregnant consumers.

show abstract

Regulation of Placental Angiogenesis

Cited by 175 publications

References 139 publications

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Role of Insulin in Placental Transport of Nutrients in Gestational Diabetes Mellitus

Influence of Maternal Angiogenic Factors During Pregnancy on Microvascular Structure in School-Age Children

Gestational exposure to titanium dioxide nanoparticles impairs the placentation through dysregulation of vascularization, proliferation and apoptosis in mice

Contact Info

Product

Resources

About