Magnetic resonance imaging of hypoxic injury to the murine placenta

Tomlinson, Tracy M.; Garbow, Joel R.; Anderson, J.; Engelbach, John A.; Nelson, D. F.; Sadovsky, Yoel

doi:10.1152/ajpregu.00425.2009

Cited by 55 publications

(37 citation statements)

References 55 publications

(58 reference statements)

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“…Moreover, there was no upregulation of placental miR-210 in response to moderate maternal hypoxia. Notably, we used a moderate level of hypoxia (O 2 =12%) because, in our previous studies, we found that this degree of hypoxia caused fetal growth restriction by 10-20%, without excessive fetal loss [16]. In addition, we initiated hypoxia at E11.5, as our goal was to assess the effect of hypoxia on the established placenta and avoid exposure to hypoxia earlier in gestation, when the feto-placental unit develops during physiological hypoxia [17-20].…”

Section: Resultsmentioning

confidence: 99%

Intact feto-placental growth in microRNA-210 deficient mice

et al. 2016

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MicroRNA-210 (miR-210) has been implicated in homeostatic adaptation during hypoxia. We hypothesized that miR-210 deficiency impacts feto-placental growth. As expected, mir-210 knockout (ko) mice exhibited markedly reduced placental miR-210 expression, compared to wild-type (wt) mice. Mating of mir-210 heterozygotes resulted in near Mendelian progeny distribution, with insignificant differences between wt and ko animals with regard to embryo or placental weight and gross morphology. Intriguingly, exposure of mice to non-severe hypoxia (O2=12%) between E11.5-E17.5 reduced placental miR-210 expression, with slight expression changes of some miR-210 target mRNAs. Thus, miR-210 is likely dispensable for feto-placental growth in normoxia or non-severe hypoxia.

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Section: Resultsmentioning

confidence: 99%

Intact feto-placental growth in microRNA-210 deficient mice

et al. 2016

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“…We also found that Fabp4 -null fetuses were indistinguishable from their wt littermates with respect to weight and morphology (not shown). Because we previously showed that human trophoblastic FABP4 is upregulated in hypoxia in vitro [21], we assessed the impact of hypoxia (O 2 =12%, E12.5–18.5) on fetal growth, using protocols previously described in our lab [30, 31]. Except for the predicted growth restriction by 10–20% of all mouse fetuses exposed to hypoxia [30, 31], there were no differences among littermates representing the different genotypes.…”

Section: Resultsmentioning

confidence: 99%

Fatty Acid Binding Protein-4 is expressed in the mouse placental labyrinth, yet is dispensable for placental triglyceride accumulation and fetal growth

Makkar¹,

Mishima²,

Chang³

et al. 2014

Placenta

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Introduction Fatty Acid Binding Protein-4 (FABP4) is a member of a family of FABP proteins that regulate intracellular lipid trafficking in diverse tissues. We recently showed that FABP4 regulates triglyceride accumulation in primary human trophoblasts. To assess the function of placental FABP4 in vivo, we tested the hypothesis that FABP4 is expressed in the murine placenta, and regulates placenta triglyceride accumulation. Methods C57Bl/6 wild type or Fabp4-null mice were time-bred, and fetuses and placentas harvested at different time points during pregnancy. Placental FABP4 expression was assessed at different gestational ages, using quantitative PCR, immunohistochemistry, immunofluorescence and western immunoblotting. FABPs expression was examined by RT-qPCR. Placental lipids were extracted using the Folch method and triglyceride levels determined using a colorimetric quantification kit. Results Using immunohistochemistry, we found that FABP4 was expressed in the placental labyrinthine layer, predominantly in endothelial cells in association with CD31 positive fetal capillaries. The level of placental FABP4 mRNA and protein increased from E12.5 to E16.5 and slightly decreased at E18.5. Breeding of Fabp4 heterozygous mice resulted in embryonic genotypes that followed a Mendelian distribution and exhibited normal weight and morphology, triglyceride content, and expression of other FABP family members. Exposure to hypoxia (O2=12%) between E12.5–E18.5 did not uncover a difference between wild type and Fabp4-null mice. Conclusions FABP4 is expressed in the mouse placental labyrinth, with highest expression at E16.5. FABP4 is dispensable for feto-placental growth and placental lipid accumulation.

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“…Trophoblast cells migrate toward oxygen in the human placental bed ( Jauniaux et al 2001 ). Alternatively, others have used in vivo chronic hypoxia to overwhelm adaptive responses and create placental injury ( Tomlinson et al 2010; Lai et al 2011 ). Thus, oxygen availability can serve as context-dependent instructive or pathological signals affecting placentation.…”

Section: Regulation Of Invasive Trophoblast Differentiationmentioning

confidence: 99%

Adaptive mechanisms controlling uterine spiral artery remodeling during the establishment of pregnancy

Soares¹,

Chakraborty²,

Kubota³

et al. 2014

Int. J. Dev. Biol.

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Implantation of the embryo into the uterus triggers the initiation of hemochorial placentation. The hemochorial placenta facilitates the acquisition of maternal resources required for embryo/fetal growth. Uterine spiral arteries form the nutrient supply line for the placenta and fetus. This vascular conduit undergoes gestation stage-specific remodeling directed by maternal natural killer cells and embryo-derived invasive trophoblast lineages. The placentation site, including remodeling of the uterine spiral arteries, is shaped by environmental challenges. In this review, we discuss the cellular participants controlling pregnancy-dependent uterine spiral artery remodeling and mechanisms responsible for their development and function.

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Magnetic resonance imaging of hypoxic injury to the murine placenta

Abstract: Tomlinson TM, Garbow JR, Anderson JR, Engelbach JA, Nelson DM, Sadovsky Y. Magnetic resonance imaging of hypoxic injury to the murine placenta.

Cited by 55 publications

References 55 publications

Intact feto-placental growth in microRNA-210 deficient mice

Intact feto-placental growth in microRNA-210 deficient mice

Fatty Acid Binding Protein-4 is expressed in the mouse placental labyrinth, yet is dispensable for placental triglyceride accumulation and fetal growth

Adaptive mechanisms controlling uterine spiral artery remodeling during the establishment of pregnancy

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