scholarly journals Molecular Patterns of Neurodevelopmental Preconditioning: A Study of the Effects of Antenatal Steroid Therapy in a Protein-Restriction Mouse Model

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Clarissa Velayo ◽  
Takuya Ito ◽  
Yupeng Dong ◽  
Miyuki Endo ◽  
Rika Sugibayashi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Microarray Analysis ◽  
Steroid Therapy ◽  
Regulatory Networks ◽  
Harmful Effect ◽  
High Stress ◽  
Protein Restriction ◽  
Late Gestation ◽  
Treatment Protocols ◽  
Antenatal Steroid

Introduction. Prenatal programming secondary to maternal protein restriction renders an inherent susceptibility to neural compromise in neonates and any addition of glucocorticosteroids results in further damage. This is an investigation of consequent global gene activity due to effects of antenatal steroid therapy on a protein restriction mouse model. Methods. C57BL/6N pregnant mice were administered control or protein restricted diets and subjected to either 100 μg/Kg of dexamethasone sodium phosphate with normosaline or normosaline alone during late gestation (E10–E17). Nontreatment groups were also included. Brain samples were collected on embryonic day 17 and analyzed by mRNA microarray analysis. Results. Microarray analyses presented 332 significantly regulated genes. Overall, neurodevelopmental genes were overrepresented and a subset of 8 genes allowed treatment segregation through the hierarchical clustering method. The addition of stress or steroids greatly affected gene regulation through glucocorticoid receptor and stress signaling pathways. Furthermore, differences between dexamethasone-administered treatments implied a harmful effect during conditions of high stress. Microarray analysis was validated using qPCR. Conclusion. The effects of antenatal steroid therapy vary in fetuses according to maternal-fetal factors and environmental stimuli. Defining the key regulatory networks that signal either beneficial or damaging corticosteroid action would result in valuable adjustments to current treatment protocols.

Effects of Antenatal Steroid Therapy on Neurodevelopment in an IUGR Mouse Model

2010 ◽  
Vol 28 (2) ◽  
pp. 79-86 ◽  
Author(s):  
Clarissa Velayo ◽  
Takuya Ito ◽  
Hiroshi Chisaka ◽  
Nobuo Yaegashi ◽  
Kunihiro Okamura ◽  
...  
Keyword(s):  
Mouse Model ◽  
Steroid Therapy ◽  
Antenatal Steroid

scholarly journals Male Fetal Sex Affects Uteroplacental Angiogenesis in Growth Restriction Mouse Model†

2021 ◽  
Author(s):  
Jessica F Hebert ◽  
Jess A Millar ◽  
Rahul Raghavan ◽  
Amie Romney ◽  
Jason E Podrabsky ◽  
...  
Keyword(s):  
Mouse Model ◽  
Killer Cell ◽  
Receptor Activation ◽  
Growth Restriction ◽  
Late Gestation ◽  
Spiral Artery ◽  
Micro Computed Tomography ◽  
Fetal Sex ◽  
Maternal Genotype ◽  
Agt Gene

Abstract Abnormally increased angiotensin II activity related to maternal angiotensinogen (AGT) genetic variants, or aberrant receptor activation, is associated with small-for-gestational-age (SGA) babies and abnormal uterine spiral artery remodeling in humans. Our group studies a murine AGT gene titration transgenic (TG; 3-copies of the AGT gene) model, which has a 20% increase in AGT expression mimicking a common human AGT genetic variant (A[−6]G) associated with intrauterine growth restriction (IUGR) and spiral artery pathology. We hypothesized that aberrant maternal AGT expression impacts pregnancy-induced uterine spiral artery angiogenesis in this mouse model leading to IUGR. We controlled for fetal sex and fetal genotype (e.g., only 2-copy wild-type [WT] progeny from WT and TG dams were included). Uteroplacental samples from WT and TG dams from early (days 6.5 and 8.5), mid (d12.5), and late (d16.5) gestation were studied to assess uterine natural killer cell (uNK) phenotypes, decidual metrial triangle angiogenic factors, placental growth and capillary density, placental transcriptomics, and placental nutrient transport. Spiral artery architecture was evaluated at day 16.5 by contrast-perfused three-dimensional micro-computed tomography (3D microCT). Our results suggest that uteroplacental angiogenesis is significantly reduced in TG dams at day 16.5. Males from TG dams are associated with significantly reduced uteroplacental angiogenesis from early to late gestation compared with their female littermates and WT controls. Angiogenesis was not different between fetal sexes from WT dams. We conclude that male fetal sex compounds the pathologic impact of maternal genotype in this mouse model of growth restriction.

scholarly journals The Liver X‐Receptor (LXR) gene promoter is hypermethylated in a mouse model of prenatal protein restriction

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Torsten Plosch ◽  
Esther M.E. Straten ◽  
Vincent W. Bloks ◽  
Nicolette C.A. Huijkman ◽  
Folkert Kuipers
Keyword(s):  
Mouse Model ◽  
Gene Promoter ◽  
Liver X Receptor ◽  
Protein Restriction

scholarly journals Identification of novel miRNA‐mRNA regulatory networks in contact dermatitis by integrated microarray analysis

Allergy ◽  
2020 ◽  
Author(s):  
Paulina Werner ◽  
Lukas Wisgrill ◽  
Matilda Riskumäki ◽  
Erja Jalonen ◽  
Johanna Vendelin ◽  
...  
Keyword(s):  
Contact Dermatitis ◽  
Microarray Analysis ◽  
Regulatory Networks ◽  
Novel Mirna

scholarly journals Pharmacologic inhibition of mTORC1 mimics dietary protein restriction in a mouse model of lactation

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Virginia L. Pszczolkowski ◽  
Steven J. Halderson ◽  
Emma J. Meyer ◽  
Amy Lin ◽  
Sebastian I. Arriola Apelo
Keyword(s):  
Mouse Model ◽  
Dietary Protein ◽  
Protein Restriction ◽  
Dietary Protein Restriction ◽  
Pharmacologic Inhibition

scholarly journals Antenatal Steroid Therapy for Fetal Lung Maturation and the Subsequent Risk of Childhood Asthma: A Longitudinal Analysis

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Jason D. Pole ◽  
Cameron A. Mustard ◽  
Teresa To ◽  
Joseph Beyene ◽  
Alexander C. Allen
Keyword(s):  
Risk Factor ◽  
Confidence Interval ◽  
Steroid Therapy ◽  
Independent Risk Factor ◽  
Cox Proportional Hazards ◽  
Hazard Ratio ◽  
Adjusted Hazard Ratio ◽  
Care Utilization ◽  
Lung Maturation ◽  
Antenatal Steroid

This study was designed to test the hypothesis that fetal exposure to corticosteroids in the antenatal period is an independent risk factor for the development of asthma in early childhood with little or no effect in later childhood. A population-based cohort study of all pregnant women who resided in Nova Scotia, Canada, and gave birth to a singleton fetus between 1989 and 1998 was undertaken. After a priori specified exclusions, 80,448 infants were available for analysis. Using linked health care utilization records, incident asthma cases developed after 36 months of age were identified. Extended Cox proportional hazards models were used to estimate hazard ratios while controlling for confounders. Exposure to corticosteroids during pregnancy was associated with a risk of asthma in childhood between 3–5 years of age: adjusted hazard ratio of 1.19 (95% confidence interval: 1.03, 1.39), with no association noted after 5 years of age: adjusted hazard ratio for 5–7 years was 1.06 (95% confidence interval: 0.86, 1.30) and for 8 or greater years was 0.74 (95% confidence interval: 0.54, 1.03). Antenatal steroid therapy appears to be an independent risk factor for the development of asthma between 3 and 5 years of age.

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