8-bromo-cyclicAMP stimulates glucose transporter-1 expression in a human choriocarcinoma cell line

Ogura, Kyoko; Sakata, Masahiro; Okamoto, Yoko; Yasui, Yuko; Tadokoro, Chikae; Yoshimoto, Yasuaki; Yamaguchi, Masatoshi; Kurachi, Hirohisa; Maeda, Toshiro; Murata, Yuji

doi:10.1677/joe.0.1640171

Cited by 50 publications

(29 citation statements)

References 38 publications

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“…cAMP treatment resulted in increased secretion of ␤-HCG into the media indicating differentiation of the BeWo cells as previously reported by others (24) and therefore served as a positive control for viability. PGH secretion was also increased by cAMP (p ϭ 0.003) (Fig.…”

Section: Resultssupporting

confidence: 66%

Regulation of Placental Growth Hormone Secretion in a Human Trophoblast Model—The Effects of Hormones and Adipokines

et al. 2008

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Placental growth hormone (PGH) is secreted from the human placental syncytiotrophoblast into the maternal circulation. PGH levels in pregnant women correlate with the birth weight of their offspring. We hypothesized that metabolic regulators may alter PGH secretion. BeWo cells as human trophoblast models were treated for 24, 48, and 72 h with insulin, insulin-like growth factor (IGF)-1, cortisol, ghrelin, leptin and visfatin. P lacental growth hormone (PGH) is synthesized in and secreted from the human placental syncytiotrophoblast (1) into the maternal circulation in a nonpulsatile manner, detectable in the maternal circulation from gestational week 5, and gradually increases in concentration throughout pregnancy. It has a short half-life and is undetectable 3 h after parturition (2). It is only found in the maternal, but not fetal circulation. Its maternal levels rise profoundly between weeks 20 and 30 of gestation, thus progressively replacing pituitary growth hormone in the human maternal circulation from midgestation onward (3-5). PGH has somatotropic effects, acting on liver and adipose tissue to influence gluconeogenesis and lipolysis to help ensure an adequate nutrient supply for the fetoplacental unit (6).Previously, our group and others have shown a positive correlation between PGH levels in pregnant women and the birth weight of their offspring, stimulating discussions about its possible impact on fetal growth (2,7). Understanding the regulation of fetal growth is important. According to the "Fetal Origins of Disease" hypothesis, it is well recognized that Type 2 diabetes mellitus (T2DM) and features of the metabolic syndrome are associated with birth weights at the extreme of the growth continuum (either small or large for gestational age) (8). The physiologic role of PGH in pregnancy is not completely understood, but its continuous secretion at high levels during pregnancy sparked speculation that it may be an important placental hormone affecting both mother and, indirectly, fetus (9). In vivo experiments have demonstrated that growth hormone, when infused into pregnant ewes late in gestation, can increase fetal growth (10). Transgenic mice overexpressing the human PGH gene become larger than their normal littermates and are hyperinsulinemic and insulin resistant (11). The relationship between fetal growth and PGH raises the possibility that PGH could be involved in the development of insulin resistance in pregnancy and might play an important role in gestational diabetes mellitus (GDM) and pregestational diabetes (12,13).The regulation of PGH secretion is very different from that of pituitary growth hormone (GH) as growth-hormone-releasing hormone does not modulate PGH in vivo. Furthermore, in vitro and in vivo studies have revealed that alterations in maternal nutrient (glucose) availability may alter PGH secretion (14). However, two decades have passed since the discovery of PGH, and still little is known about the regulation of its secretion.We hypothesized that PGH secretion is regul...

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Section: Resultssupporting

confidence: 66%

Regulation of Placental Growth Hormone Secretion in a Human Trophoblast Model—The Effects of Hormones and Adipokines

et al. 2008

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“…We found that a mixed population of cells did not transcytose virus as effectively as a monolayer of undifferentiated cells. This may be due to changes in BeWo cellular protein expression accompanying maturation that reduced virus attachment and transport (33,35,39,43). As transport of molecules across the maternal-fetal barrier must continue to take place throughout pregnancy, it is likely that specific cell factors play a role in HBV transport and that these change with cellular differentiation.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B Virus Translocates across a Trophoblastic Barrier

Bhat

Anderson

2007

J Virol

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Mother-infant transmission of hepatitis B virus (HBV) accounts for up to 30% of worldwide chronic infections. The mechanism and high-risk period of HBV transmission from mother to infant are unknown. Although largely prevented by neonatal vaccination, significant transmission continues to occur in high-risk populations. It is unclear whether HBV can traverse an intact epithelial barrier to infect a new host. Transplacental transmission of a number of viruses relies on transcytotic pathways across placental cells. We wished to determine whether infectious HBV can traverse a polarized trophoblast monolayer. We used a human placenta-derived cell line, BeWo, cultured on membranes as polarized monolayers, to model the maternal-fetal barrier. We assessed the effects of placental maturity and maternal immunoglobulin on viral transport. Intracellular viral trafficking pathways were investigated by confocal microscopy. Free HBV (and infectious duck hepatitis B virus) transcytosed across trophoblastic cells at a rate of 5% in 30 min. Viral transport occurred in microtubule-dependent endosomal vesicles. Additionally, confocal microscopy showed that the internalized virus traverses a monensin-sensitive endosomal compartment. Differentiation of the cytotrophoblasts to syncytiotrophoblasts resulted in a 25% reduction in viral transcytosis, suggesting that placental maturity may protect the fetus. Virus translocation was also reduced in the presence of HBV immunoglobulin. We show for the first time that transcytosis of infectious hepadnavirus can occur across a trophoblastic barrier early in gestation, with the risk of transmission being reduced by placental maturity and specific maternal antibody. This study suggests a mechanism by which mother-infant transmission may occur.

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“…There are numerous pathways linking changes in cAMP to effects on glucose metabolism. For example chronic treatment with cAMP analogues increased glucose utilization by up-regulating GLUT-1 expression in human choriocarcinoma cells (68), although opposite results were observed in primary mouse placental cells (69). In insulin-sensitive tissues, several studies have shown that glucose uptake was enhanced by regulation of GLUT-1 expression through the cAMP/protein kinase A pathway.…”

Section: Fig 6 Effect Of Pio On Glut-1 Expressionmentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor γ Thiazolidinedione Agonists Increase Glucose Metabolism in Astrocytes

Russo

Gavrilyuk

Weinberg

et al. 2003

Journal of Biological Chemistry

151

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Activation of peroxisome proliferator-activated receptors (PPARs) can regulate brain physiology and provide protection in models of neurological disease; however, neither their exact targets nor mechanisms of action in brain are known. In many cells, PPAR␥ agonists increase glucose uptake and metabolism. Because astrocytes store glucose and provide lactate to neurons on demand, we tested effects of PPAR␥ agonists on astroglial glucose metabolism. Incubation of cortical astrocytes with the PPAR␥ thiazolidinedione (TZD) agonist pioglitazone (Pio) significantly increased glucose consumption in a time-and dose-dependent manner, with maximal increase of 36% observed after 4 h in 30 M Pio. Pio increased 2-deoxy-glucose uptake because of increased flux through the type 1 glucose transporter. However, at this time point Pio did not increase type 1 glucose transporter expression, nor were its effects blocked by transcriptional or translational inhibitors. Pio also increased astrocyte lactate production as soon as 3 h after incubation. These effects were replicated by other TZDs; however, the order of efficacy (troglitazone > pioglitazone > rosiglitazone) suggests that effects were not mediated via PPAR␥ activation. TZDs increased astrocyte cAMP levels, and their glucose modifying effects were reduced by protein kinase A inhibitors. TZDs inhibited state III respiration in isolated brain mitochondria, whereas in astrocytes they caused mitochondrial membrane hyperpolarization. Pio protected astrocytes against hypoglycemia-induced cell death. Finally, glucose uptake was modified in brain sections prepared from Pio-fed rats. These results demonstrate that TZDs modify astrocyte metabolism and mitochondrial function, which could be beneficial in neurological conditions where glucose availability is reduced.

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8-bromo-cyclicAMP stimulates glucose transporter-1 expression in a human choriocarcinoma cell line

Cited by 50 publications

References 38 publications

Regulation of Placental Growth Hormone Secretion in a Human Trophoblast Model—The Effects of Hormones and Adipokines

Regulation of Placental Growth Hormone Secretion in a Human Trophoblast Model—The Effects of Hormones and Adipokines

Hepatitis B Virus Translocates across a Trophoblastic Barrier

Peroxisome Proliferator-activated Receptor γ Thiazolidinedione Agonists Increase Glucose Metabolism in Astrocytes

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