T Cotechini1, W J Hopman2, C H Graham3. 1. Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada. Electronic address: 4tc16@queensu.ca. 2. Clinical Research Centre, Kingston General Hospital, Kingston, Ontario, Canada; Department of Public Health Sciences, Queen's University, Kingston, Ontario, Canada. 3. Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario K7L 3N6, Canada. Electronic address: grahamc@queensu.ca.
Abstract
INTRODUCTION: Evidence links alterations in placental shape and size to fetal growth restriction (FGR). Here we determined whether alterations in placental morphometrics are linked to FGR induced by abnormal maternal inflammation. METHODS: We used an inflammation-induced model of FGR in which pregnant rats receive lipopolysaccharide (LPS) on gestational days (GD) 13.5-16.5. Fetal weights were matched to various parameters of placental morphometrics including weight, area, minor and major axes lengths and thickness. RESULTS: Compared with saline administration, LPS administration was associated with altered placental morphometrics, including reduced placental weight, decreased placental area and a trend towards reduced placental thickness. When data were dichotomized as FGR or normal-sized fetuses within treatment groups, a significant increase in the placental-weight-to-fetal-weight ratio and placental thickness was observed only in the saline-associated FGR subgroup. Multivariable linear regression revealed that the lengths of the major and minor placental axes were predictors of fetal weight, regardless of treatment modality. Subgroup regression analysis by treatment revealed that the lengths of the major and minor placental axes were predictors of fetal weight in the saline-treatment group while only the minor placental axis was a predictor of fetal weight in the LPS cohort. Finally, placental area and the length of the minor placental axis were correlated with implantation site location only in the saline-treatment group. DISCUSSION/ CONCLUSION: These findings indicate that inflammation-induced FGR is associated with alterations in placental morphometrics. Our data reveal that the mechanisms leading to inflammation-induced FGR may be different from the mechanisms leading to idiopathic FGR.
INTRODUCTION: Evidence links alterations in placental shape and size to fetal growth restriction (FGR). Here we determined whether alterations in placental morphometrics are linked to FGR induced by abnormal maternal inflammation. METHODS: We used an inflammation-induced model of FGR in which pregnant rats receive lipopolysaccharide (LPS) on gestational days (GD) 13.5-16.5. Fetal weights were matched to various parameters of placental morphometrics including weight, area, minor and major axes lengths and thickness. RESULTS: Compared with saline administration, LPS administration was associated with altered placental morphometrics, including reduced placental weight, decreased placental area and a trend towards reduced placental thickness. When data were dichotomized as FGR or normal-sized fetuses within treatment groups, a significant increase in the placental-weight-to-fetal-weight ratio and placental thickness was observed only in the saline-associated FGR subgroup. Multivariable linear regression revealed that the lengths of the major and minor placental axes were predictors of fetal weight, regardless of treatment modality. Subgroup regression analysis by treatment revealed that the lengths of the major and minor placental axes were predictors of fetal weight in the saline-treatment group while only the minor placental axis was a predictor of fetal weight in the LPS cohort. Finally, placental area and the length of the minor placental axis were correlated with implantation site location only in the saline-treatment group. DISCUSSION/ CONCLUSION: These findings indicate that inflammation-induced FGR is associated with alterations in placental morphometrics. Our data reveal that the mechanisms leading to inflammation-induced FGR may be different from the mechanisms leading to idiopathic FGR.
Authors: Caitlin N Cadaret; Elena M Merrick; Taylor L Barnes; Kristin A Beede; Robert J Posont; Jessica L Petersen; Dustin T Yates Journal: J Anim Sci Date: 2019-12-17 Impact factor: 3.159
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Authors: Caitlin N Cadaret; Robert J Posont; Kristin A Beede; Hannah E Riley; John Dustin Loy; Dustin T Yates Journal: Transl Anim Sci Date: 2019-04-03