Sex specific changes in placental growth and MAPK following short term maternal dexamethasone exposure in the mouse
Author(s)
Cuffe, JSM
Dickinson, H
Simmons, DG
Moritz, KM
Griffith University Author(s)
Year published
2011
Metadata
Show full item recordAbstract
Objectives: Maternal glucocorticoid (GC) exposure during pregnancy can alter fetal development and
program the onset of disease in adult offspring. The placenta helps protect the fetus from excess GC
exposure but is itself susceptible to maternal insults and may be involved in sex dependant regulation of
fetal programming. This study aimed to investigate the effects of maternal GC exposure on the developing
placenta.
Study design and main outcome measures: Pregnant mice were treated with dexamethasone (DEX-1 mg/
kg/h) or saline (SAL) for 60 h via minipump beginning at E12.5. Placentas were collected at E14.5 and
E17.5 and ...
View more >Objectives: Maternal glucocorticoid (GC) exposure during pregnancy can alter fetal development and program the onset of disease in adult offspring. The placenta helps protect the fetus from excess GC exposure but is itself susceptible to maternal insults and may be involved in sex dependant regulation of fetal programming. This study aimed to investigate the effects of maternal GC exposure on the developing placenta. Study design and main outcome measures: Pregnant mice were treated with dexamethasone (DEX-1 mg/ kg/h) or saline (SAL) for 60 h via minipump beginning at E12.5. Placentas were collected at E14.5 and E17.5 and the expression of growth factors and placental transporters examined by real-time PCR and/or Western blot. Histological analysis was performed to assess for morphological changes. Results: At E14.5, DEX exposed male and female fetuses had a lower weight compared to SAL animals but placental weight was lower in females only. Hsd11b2 and Vegfa gene expression was increased and MAPK1 protein expression decreased in the placentas of females only. At E17.5 placental and fetal body weights were similar and differences in MAPK were no longer present although HSD11B2 protein was elevated in placentas of DEX females. Levels of glucose or amino acid transporters were unaffected. Conclusions: Results suggest sex specific responses to maternal GCs within the placenta. Decreased levels of MAPK protein in placentas of female fetuses suggest alterations in the MAPK pathway may contribute to the lower placental weights in this sex. This may contribute towards sex specific fetal programming of adult disease.
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View more >Objectives: Maternal glucocorticoid (GC) exposure during pregnancy can alter fetal development and program the onset of disease in adult offspring. The placenta helps protect the fetus from excess GC exposure but is itself susceptible to maternal insults and may be involved in sex dependant regulation of fetal programming. This study aimed to investigate the effects of maternal GC exposure on the developing placenta. Study design and main outcome measures: Pregnant mice were treated with dexamethasone (DEX-1 mg/ kg/h) or saline (SAL) for 60 h via minipump beginning at E12.5. Placentas were collected at E14.5 and E17.5 and the expression of growth factors and placental transporters examined by real-time PCR and/or Western blot. Histological analysis was performed to assess for morphological changes. Results: At E14.5, DEX exposed male and female fetuses had a lower weight compared to SAL animals but placental weight was lower in females only. Hsd11b2 and Vegfa gene expression was increased and MAPK1 protein expression decreased in the placentas of females only. At E17.5 placental and fetal body weights were similar and differences in MAPK were no longer present although HSD11B2 protein was elevated in placentas of DEX females. Levels of glucose or amino acid transporters were unaffected. Conclusions: Results suggest sex specific responses to maternal GCs within the placenta. Decreased levels of MAPK protein in placentas of female fetuses suggest alterations in the MAPK pathway may contribute to the lower placental weights in this sex. This may contribute towards sex specific fetal programming of adult disease.
View less >
Journal Title
Placenta
Volume
32
Issue
12
Subject
Biochemistry and cell biology
Clinical sciences
Clinical sciences not elsewhere classified