The Experts below are selected from a list of 618 Experts worldwide ranked by ideXlab platform
Deborah M Sloboda - One of the best experts on this subject based on the ideXlab platform.
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growth restricting effects of a single course of antenatal betamethasone treatment and the role of human Placental Lactogen
Placenta, 2013Co-Authors: Thorsten Braun, A Husar, J R G Challis, J W Dudenhausen, W Henrich, Andreas Plagemann, Deborah M SlobodaAbstract:Abstract Betamethasone (BET) is a widely used treatment for women who are at high risk of preterm delivery. In sheep, BET-induced growth restriction was found to be associated with reduced Placenta Lactogen (PL), a key regulator of fetal growth. We therefore hypothesized that also in humans a single course of BET administration is associated with a reduction of PL, associated with a deceleration in fetal growth. Objective To investigate effects of a single course of antenatal BET in humans on birth weight and PL. Methods Women exposed to BET (2 × 12 mg; n = 44) with normally grown fetuses between 23 + 5 and 34 + 0 wks (weeks + days of gestation) who delivered between 23 + 5 to 42 + 0 wks were compared to gestational age-matched controls ( n = 49). Maternal gestational blood samples were obtained before, during and after BET treatment and at the time of birth. Main outcome measures BET effects on fetal anthropometrics, Placental morphometry and Placental PL-protein and maternal plasma levels. Results The mean duration of days between BET administration and birth was 52 days. BET treatment was associated with decreased birth weight (−18.2%), head circumference (−8.6%), body length (−6.0%), and Placental width (−5.5%), as compared to controls. These changes were irrespective of possible maternal confounders (gestational age at birth, maternal age, maternal BMI gain during pregnancy, smoking etc.). However, neither PL-plasma levels within 48 h after BET treatment nor Placental PL-protein levels and maternal plasma levels at birth were changed after BET treatment. In central regions of the Placenta, BET treatment increased the circumference of syncytiotrophoblast nuclei by +4.7% and nucleus surface area by +9.4% compared to controls, but these changes were not related to Placental PL-protein or maternal PL-plasma levels at birth. Conclusion A single course of BET treatment was accompanied with reduced fetal growth, but this growth restricting effect was not associated with altered Placental or maternal plasma PL levels. Altered expression of PL appears not to be causal for BET-induced fetal growth restriction in the human.
K Bridget Brosnihan - One of the best experts on this subject based on the ideXlab platform.
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Angiotensin II and angiotensin-(1-7) decrease sFlt1 release in normal but not preeclamptic chorionic villi: an in vitro study
Reproductive Biology and Endocrinology, 2010Co-Authors: Lauren Anton, David C Merrill, Liomar Aa Neves, Courtney Gruver, Cheryl Moorefield, K Bridget BrosnihanAbstract:Background During preeclampsia, Placental angiogenesis is impaired. Factors released from the Placenta including vascular endothelial growth factor (VEGF), Placental growth factor (PLGF), soluble VEGF receptor 1 (sFlt1), and soluble endoglin (sEng) are regulatory molecules of Placental development and function. While the renin angiotensin system has been shown to regulate angiogenic factors in other research fields, these mechanisms have not been extensively studied during pregnancy. Methods We evaluated the effects of angiotensin II (Ang II) and angiotensin-(1-7) [Ang-(1-7)] on the release of VEGF, PLGF, sFlt1, and sEng from Placental chorionic villi (CV). CV were collected from nulliparous third-trimester normotensive and preeclamptic subjects. CV were incubated for 0, 2, 4, and 16 hours with or without Ang II (1 nM and 1 microM) or Ang-(1-7) (1 nM and 1 microM). The release of VEGF, PLGF, sFlt1, sEng, lactate dehydrogenase (LDH), and human Placenta Lactogen (HPL) was measured by ELISA. Results The release of sFlt1, PLGF, sEng from normal and preeclamptic CV increased over time. Release of sFlt1 and sEng was significantly higher from preeclamptic CV. VEGF was below the detectable level of the assay in normal and preeclamptic CV. After 2 hours, sFlt1 release from normal CV was significantly inhibited with Ang II (1 nM and 1 microM) and Ang-(1-7) (1 nM and 1 microM). There was a time-dependent increase in HPL indicating that the CV were functioning normally. Conclusions Our study demonstrates a critical inhibitory role of angiotensin peptides on sFlt1 in normal pregnancy. Loss of this regulation in preeclampsia may allow sFlt1 to increase resulting in anti-angiogenesis and end organ damage in the mother.
Thorsten Braun - One of the best experts on this subject based on the ideXlab platform.
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growth restricting effects of a single course of antenatal betamethasone treatment and the role of human Placental Lactogen
Placenta, 2013Co-Authors: Thorsten Braun, A Husar, J R G Challis, J W Dudenhausen, W Henrich, Andreas Plagemann, Deborah M SlobodaAbstract:Abstract Betamethasone (BET) is a widely used treatment for women who are at high risk of preterm delivery. In sheep, BET-induced growth restriction was found to be associated with reduced Placenta Lactogen (PL), a key regulator of fetal growth. We therefore hypothesized that also in humans a single course of BET administration is associated with a reduction of PL, associated with a deceleration in fetal growth. Objective To investigate effects of a single course of antenatal BET in humans on birth weight and PL. Methods Women exposed to BET (2 × 12 mg; n = 44) with normally grown fetuses between 23 + 5 and 34 + 0 wks (weeks + days of gestation) who delivered between 23 + 5 to 42 + 0 wks were compared to gestational age-matched controls ( n = 49). Maternal gestational blood samples were obtained before, during and after BET treatment and at the time of birth. Main outcome measures BET effects on fetal anthropometrics, Placental morphometry and Placental PL-protein and maternal plasma levels. Results The mean duration of days between BET administration and birth was 52 days. BET treatment was associated with decreased birth weight (−18.2%), head circumference (−8.6%), body length (−6.0%), and Placental width (−5.5%), as compared to controls. These changes were irrespective of possible maternal confounders (gestational age at birth, maternal age, maternal BMI gain during pregnancy, smoking etc.). However, neither PL-plasma levels within 48 h after BET treatment nor Placental PL-protein levels and maternal plasma levels at birth were changed after BET treatment. In central regions of the Placenta, BET treatment increased the circumference of syncytiotrophoblast nuclei by +4.7% and nucleus surface area by +9.4% compared to controls, but these changes were not related to Placental PL-protein or maternal PL-plasma levels at birth. Conclusion A single course of BET treatment was accompanied with reduced fetal growth, but this growth restricting effect was not associated with altered Placental or maternal plasma PL levels. Altered expression of PL appears not to be causal for BET-induced fetal growth restriction in the human.
Lauren Anton - One of the best experts on this subject based on the ideXlab platform.
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Angiotensin II and angiotensin-(1-7) decrease sFlt1 release in normal but not preeclamptic chorionic villi: an in vitro study
Reproductive Biology and Endocrinology, 2010Co-Authors: Lauren Anton, David C Merrill, Liomar Aa Neves, Courtney Gruver, Cheryl Moorefield, K Bridget BrosnihanAbstract:Background During preeclampsia, Placental angiogenesis is impaired. Factors released from the Placenta including vascular endothelial growth factor (VEGF), Placental growth factor (PLGF), soluble VEGF receptor 1 (sFlt1), and soluble endoglin (sEng) are regulatory molecules of Placental development and function. While the renin angiotensin system has been shown to regulate angiogenic factors in other research fields, these mechanisms have not been extensively studied during pregnancy. Methods We evaluated the effects of angiotensin II (Ang II) and angiotensin-(1-7) [Ang-(1-7)] on the release of VEGF, PLGF, sFlt1, and sEng from Placental chorionic villi (CV). CV were collected from nulliparous third-trimester normotensive and preeclamptic subjects. CV were incubated for 0, 2, 4, and 16 hours with or without Ang II (1 nM and 1 microM) or Ang-(1-7) (1 nM and 1 microM). The release of VEGF, PLGF, sFlt1, sEng, lactate dehydrogenase (LDH), and human Placenta Lactogen (HPL) was measured by ELISA. Results The release of sFlt1, PLGF, sEng from normal and preeclamptic CV increased over time. Release of sFlt1 and sEng was significantly higher from preeclamptic CV. VEGF was below the detectable level of the assay in normal and preeclamptic CV. After 2 hours, sFlt1 release from normal CV was significantly inhibited with Ang II (1 nM and 1 microM) and Ang-(1-7) (1 nM and 1 microM). There was a time-dependent increase in HPL indicating that the CV were functioning normally. Conclusions Our study demonstrates a critical inhibitory role of angiotensin peptides on sFlt1 in normal pregnancy. Loss of this regulation in preeclampsia may allow sFlt1 to increase resulting in anti-angiogenesis and end organ damage in the mother.
Andreas Plagemann - One of the best experts on this subject based on the ideXlab platform.
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growth restricting effects of a single course of antenatal betamethasone treatment and the role of human Placental Lactogen
Placenta, 2013Co-Authors: Thorsten Braun, A Husar, J R G Challis, J W Dudenhausen, W Henrich, Andreas Plagemann, Deborah M SlobodaAbstract:Abstract Betamethasone (BET) is a widely used treatment for women who are at high risk of preterm delivery. In sheep, BET-induced growth restriction was found to be associated with reduced Placenta Lactogen (PL), a key regulator of fetal growth. We therefore hypothesized that also in humans a single course of BET administration is associated with a reduction of PL, associated with a deceleration in fetal growth. Objective To investigate effects of a single course of antenatal BET in humans on birth weight and PL. Methods Women exposed to BET (2 × 12 mg; n = 44) with normally grown fetuses between 23 + 5 and 34 + 0 wks (weeks + days of gestation) who delivered between 23 + 5 to 42 + 0 wks were compared to gestational age-matched controls ( n = 49). Maternal gestational blood samples were obtained before, during and after BET treatment and at the time of birth. Main outcome measures BET effects on fetal anthropometrics, Placental morphometry and Placental PL-protein and maternal plasma levels. Results The mean duration of days between BET administration and birth was 52 days. BET treatment was associated with decreased birth weight (−18.2%), head circumference (−8.6%), body length (−6.0%), and Placental width (−5.5%), as compared to controls. These changes were irrespective of possible maternal confounders (gestational age at birth, maternal age, maternal BMI gain during pregnancy, smoking etc.). However, neither PL-plasma levels within 48 h after BET treatment nor Placental PL-protein levels and maternal plasma levels at birth were changed after BET treatment. In central regions of the Placenta, BET treatment increased the circumference of syncytiotrophoblast nuclei by +4.7% and nucleus surface area by +9.4% compared to controls, but these changes were not related to Placental PL-protein or maternal PL-plasma levels at birth. Conclusion A single course of BET treatment was accompanied with reduced fetal growth, but this growth restricting effect was not associated with altered Placental or maternal plasma PL levels. Altered expression of PL appears not to be causal for BET-induced fetal growth restriction in the human.