Improvement of insulin sensitivity promotes extravillous trophoblast cell migration stimulated by insulin-like growth factor-I

Mayama, Reiko; Izawa, Tomoko; Sakai, Kiyofumi; Suciu, Nicolae; Iwashita, M.

doi:10.1507/endocrj.ej12-0241

Cited by 29 publications

(27 citation statements)

References 30 publications

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“…Hyperphosphorylation of maternal plasma IGFBP-1 may serve as a novel early biomarker of IUGR. These observations are consistent with the possibility that IGFBP-1 phosphorylation constitutes a link between decreased decidual oxygen and nutrient availability and reduced fetal growth, mediated by diminished IGF-I bioavailability, resulting in inhibition of trophoblast invasion [125,148,149] and placental function (Figure 4).…”

Section: Mechanistic Tor Functions As a Decidual Nutrient Sensor And supporting

confidence: 85%

Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†

Gupta

Jansson

2018

Biology of Reproduction

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Mechanistic target of rapamycin (mTOR) signaling functions as a central regulator of cellular metabolism, growth, and survival in response to hormones, growth factors, nutrients, energy, and stress signals. Mechanistic TOR is therefore critical for the growth of most fetal organs, and global mTOR deletion is embryonic lethal. This review discusses emerging evidence suggesting that mTOR signaling also has a role as a critical hub in the overall homeostatic control of fetal growth, adjusting the fetal growth trajectory according to the ability of the maternal supply line to support fetal growth. In the fetus, liver mTOR governs the secretion and phosphorylation of insulin-like growth factor binding protein 1 (IGFBP-1) thereby controlling the bioavailability of insulin-like growth factors (IGF-I and IGF-II), which function as important growth hormones during fetal life. In the placenta, mTOR responds to a large number of growth-related signals, including amino acids, glucose, oxygen, folate, and growth factors, to regulate trophoblast mitochondrial respiration, nutrient transport, and protein synthesis, thereby influencing fetal growth. In the maternal compartment, mTOR is an integral part of a decidual nutrient sensor which links oxygen and nutrient availability to the phosphorylation of IGFBP-1 with preferential effects on the bioavailability of IGF-I in the maternal–fetal interface and in the maternal circulation. These new roles of mTOR signaling in the regulation fetal growth will help us better understand the molecular underpinnings of abnormal fetal growth, such as intrauterine growth restriction and fetal overgrowth, and may represent novel avenues for diagnostics and intervention in important pregnancy complications.

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Section: Mechanistic Tor Functions As a Decidual Nutrient Sensor And supporting

confidence: 85%

Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†

Gupta

Jansson

2018

Biology of Reproduction

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“…; Mayama et al . ). However, IGF2 may also signal via IGF2R and G i proteins, MAPK and Rho GTPase pathways to trigger trophoblast migration and invasion (McKinnon et al .…”

Section: Introductionmentioning

confidence: 97%

Placental phenotype and the insulin‐like growth factors: resource allocation to fetal growth

Sferruzzi‐Perri

Sandovici²,

Constância³

et al. 2017

The Journal of Physiology

142

128

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The placenta is the main determinant of fetal growth and development in utero. It supplies all the nutrients and oxygen required for fetal growth and secretes hormones that facilitate maternal allocation of nutrients to the fetus. Furthermore, the placenta responds to nutritional and metabolic signals in the mother by altering its structural and functional phenotype, which can lead to changes in maternal resource allocation to the fetus. The molecular mechanisms by which the placenta senses and responds to environmental cues are poorly understood. This review discusses the role of the insulin-like growth factors (IGFs) in controlling placental resource allocation to fetal growth, particularly in response to adverse gestational environments. In particular, it assesses the impact of the IGFs and their signalling machinery on placental morphogenesis, substrate transport and hormone secretion, primarily in the laboratory species, although it draws on data from human and other species where relevant. It also considers the role of the IGFs as environmental signals in linking resource availability to fetal growth through changes in the morphological and functional phenotype of the placenta. As altered fetal growth is associated with increased perinatal morbidity and mortality and a greater risk of developing adult-onset diseases in later life, understanding the role of IGFs during pregnancy in regulating placental resource allocation to fetal growth is important for identifying the mechanisms underlying the developmental programming of offspring phenotype by suboptimal intrauterine growth.

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“…Insufficient extravillous trophoblast invasion of the endometrium has been reported to cause pregnancy-associated complications, including miscarriage, pregnancy-induced hypertension and fetal growth restriction (36). Moreover, the migration and invasion of trophoblast cells has been suggested to be associated with insulin resistance (37). The results of the present study suggested that miR-345-3p expression decreased in GDM maternal placenta tissue and blood.…”

Section: Discussionmentioning

confidence: 47%

miR‑345‑3p serves a protective role during gestational diabetes mellitus by targeting BAK1

Zhuang

2020

Exp Ther Med

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Recent studies have demonstrated that microRNAs (miRs) serve a crucial role during the development of gestational diabetes mellitus (GDM). However, the mechanisms underlying miR-345-3p and its protective role during GDM have not been previously reported. The present study investigated miR-345-3p expression and function in vitro, and the possible molecular mechanisms underlying GDM. Compared with healthy pregnant women, miR-345-3p was downregulated in the placental tissue and peripheral blood of patients with GDM. Further investigation revealed that BCL2-antagonist/killer 1 (BAK1) was a predicted target gene of miR-345-3p, and the expression of BAK1 was significantly increased in patients with GDM compared with healthy pregnant women. In vitro analysis revealed that miR-345-3p mimic significantly increased cell viability, migration and invasion, inhibited apoptosis, upregulated Bcl-2 and matrix metallopeptidase 9 expression, and decreased Bax expression compared with the control group. Furthermore, miR-245-3p mimic-induced alterations were reversed by BAK1 overexpression. The results suggested that miR-345-3p overexpression exhibited a protective role in patients with GDM by inhibiting HTR8-/SVneo cell apoptosis, and promoting cell proliferation and migration via targeting BAK1. The use of miR-345-3p for the diagnosis of GDM requires further investigation.

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Improvement of insulin sensitivity promotes extravillous trophoblast cell migration stimulated by insulin-like growth factor-I

Cited by 29 publications

References 30 publications

Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†

Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†

Placental phenotype and the insulin‐like growth factors: resource allocation to fetal growth

miR‑345‑3p serves a protective role during gestational diabetes mellitus by targeting BAK1

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