Effects of diacylglycerol and gonadotropin-releasing hormone on human chorionic gonadotropin release by cultured trophoblast cells

Iwashita, Mitsutoshi; Watanabe, Miki; Setoyama, Takuya; Mimuro, T.; Nakayamab, Setsuko; Adachi, Tomoko; Takeda, Yoshihiko; Sakamoto, Shoichi

doi:10.1016/0143-4004(92)90036-s

Cited by 16 publications

(3 citation statements)

References 28 publications

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“…The process by which this occurs in yet unknown. Hormone production appears responsive to signal transduction through membrane-bound phospholipase C and protein kinase C [43,44]. Sera containing aPL antibodies can effectively block the induction of hCG production by exogenous phospholipase C or by GnRH [45,46].…”

Section: Discussionmentioning

confidence: 98%

Monoclonal Antibody against Phosphatidylserine Inhibits in Vitro Human Trophoblastic Hormone Production and Invasion1

Katsuragawa

Kanzaki

Inoue

et al. 1997

Biology of Reproduction

152

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Naturally occurring antiphospholipid (aPL) antibodies against cardiolipin (CL)- and phosphatidylserine (PS)-dependent antigens are associated with placental dysfunction and unsuccessful pregnancy. Murine monoclonal aPL antibodies react with placental trophoblast and may interfere with normal trophoblastic function. In this study, we evaluated the expression of phospholipid-dependent antigens during trophoblast differentiation and measured the effects of monoclonal aPL antibodies on two in vitro aspects of trophoblast differentiation: hormone production and invasion into filters coated with extracellular matrix. Murine monoclonal IgM aPL antibodies that differentiated between PS and CL were used: 3SB9b reacted only with PS (CL-/PS+), D11A4 reacted only with CL (CL+/PS-), and BA3B5C4 reacted with both CL and PS (CL+/PS+). Isolated trophoblasts were cultured for 4 days, and reactivity with monoclonal aPL antibodies was evaluated daily. BA3B5C4 (CL+/PS+) reacted strongly with most trophoblasts that were freshly isolated (Day 0) and through 2 days of culture, after which time the percentage of cells reactive with BA3B5C4 decreased steadily. 3SB9b (CL-/PS+) reactivity increased during incubation; about 8% of cells reacted initially, but after 1 day of incubation 100% reacted, and this percentage remained stable throughout the 4-day incubation. D11A4 (CL+/PS-) reacted only minimally and at the level of the negative control monoclonal antibody (mAb) with 1- and 2-day cultures. Both mAbs that reacted with PS-dependent antigens completely prevented invasion of matrigel-coated filters by isolated trophoblasts. These mAbs also inhibited trophoblastic hCG and human PL production by more than 45%. Thus, as trophoblasts undergo differentiation, they are reactive with mAbs against PS. These antibodies are inhibitory in vitro to trophoblastic hormone production and invasion.

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Section: Discussionmentioning

confidence: 98%

Monoclonal Antibody against Phosphatidylserine Inhibits in Vitro Human Trophoblastic Hormone Production and Invasion1

Katsuragawa

Kanzaki

Inoue

et al. 1997

Biology of Reproduction

152

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“…Female-specific associations of 13 C-PA DGs with glycemia (2 h) and BMI and between 13 C-OA LPC and LPE with maternal BMI may also suggest that alterations in these important lipid signaling molecules [ 55 , 56 , 57 , 58 , 59 ] may also be part of a sex-specific adaptive strategy. Placental DGs are known to induce the release of human chorionic gonadotropin and placental lactogen [ 60 , 61 , 62 ] and stimulate the production of progesterone [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Sex-Dependent Regulation of Placental Oleic Acid and Palmitic Acid Metabolism by Maternal Glycemia and Associations with Birthweight

Watkins

Yong

Mah

et al. 2022

IJMS

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Pregnancy complications such as maternal hyperglycemia increase perinatal mortality and morbidity, but risks are higher in males than in females. We hypothesized that fetal sex-dependent differences in placental palmitic-acid (PA) and oleic-acid (OA) metabolism influence such risks. Placental explants (n = 22) were incubated with isotope-labeled fatty acids (13C-PA or 13C-OA) for 24 or 48 h and the production of forty-seven 13C-PA lipids and thirty-seven 13C-OA lipids quantified by LCMS. Linear regression was used to investigate associations between maternal glycemia, BMI and fetal sex with 13C lipids, and between 13C lipids and birthweight centile. Placental explants from females showed greater incorporation of 13C-OA and 13C-PA into almost all lipids compared to males. Fetal sex also influenced relationships with maternal glycemia, with many 13C-OA and 13C-PA acylcarnitines, 13C-PA-diacylglycerols and 13C-PA phospholipids positively associated with glycemia in females but not in males. In contrast, several 13C-OA triacylglycerols and 13C-OA phospholipids were negatively associated with glycemia in males but not in females. Birthweight centile in females was positively associated with six 13C-PA and three 13C-OA lipids (mainly acylcarnitines) and was negatively associated with eight 13C-OA lipids, while males showed few associations. Fetal sex thus influences placental lipid metabolism and could be a key modulator of the impact of maternal metabolic health on perinatal outcomes, potentially contributing toward sex-specific adaptions in which females prioritize survival.

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“…Activation of the DAG-PKC pathway associated with abnormal growth and differentiation during diabetic embryopathy has not previously been demonstrated. Several PKC isotypes have been detected in the placenta and decidua of the human and the rat (35)(36)(37)(38)(39). In the human placenta, there are significant increases in PKC ␤II and ⑀ on the microvillus membrane and in PKC ␥ and ⑀ on the basal membrane between 16 and 40 weeks of gestation (40).…”

Section: Discussionmentioning

confidence: 99%

Diacylglycerol Production and Protein Kinase C Activity Are Increased in a Mouse Model of Diabetic Embryopathy

et al. 2002

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Activation of the diacylglycerol-protein kinase C (DAG-PKC) cascade by excess glucose has been implicated in vascular complications of diabetes. Its involvement in diabetic embryopathy has not been established. We examined DAG production and PKC activities in embryos and decidua of streptozotocin (STZ)-diabetic or transiently hyperglycemic mice during neural tube formation. STZ diabetes significantly increased DAG and total PKC activity in decidua (1.5-and 1.4-fold, respectively) and embryos (1.7-and 1.3-fold, respectively) on day 9.5. Membrane-associated PKC ␣, ␤II, ␦, and were increased in decidua by 1.25-to 2.8-fold. Maternal hyperglycemia induced by glucose injection on day 7.5, the day before the onset of neural tube formation, also increased DAG, PKC activity, and PKC isoforms (1.1-, 1.6-, and 1.5-fold, respectively) in the embryo on day 9.5. Notably, membrane-associated PKC activity was increased 24-fold in embryos of diabetic mice with structural defects. These data indicate that hyperglycemia just before organogenesis activates the DAG-PKC cascade and is correlated with congenital defects.

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Effects of diacylglycerol and gonadotropin-releasing hormone on human chorionic gonadotropin release by cultured trophoblast cells

Cited by 16 publications

References 28 publications

Monoclonal Antibody against Phosphatidylserine Inhibits in Vitro Human Trophoblastic Hormone Production and Invasion1

Monoclonal Antibody against Phosphatidylserine Inhibits in Vitro Human Trophoblastic Hormone Production and Invasion1

Sex-Dependent Regulation of Placental Oleic Acid and Palmitic Acid Metabolism by Maternal Glycemia and Associations with Birthweight

Diacylglycerol Production and Protein Kinase C Activity Are Increased in a Mouse Model of Diabetic Embryopathy

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