Altered gene expression in human placenta after suspected preterm labour

Strunk, Mark; Breton, Paula; Paulés, Cristina; Benito, Rafael; Moreno, Elena Álvarez; Garcés, María Fernanda; Godino, Javier; Schoorlemmer, Jon

doi:10.1016/j.placenta.2017.04.025

Cited by 19 publications

(22 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…33,34 Furthermore, the increase in maternal serum cytokines is mirrored in the cytokine levels within the placental tissue. 34 However, no elevation was seen within the amniotic fluid (Figure 2B). The human placenta has the capacity to both produce and express virtually all known cytokines.…”

Section: | Discussionmentioning

confidence: 99%

Lipopolysaccharide‐induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Fricke

Elgin

Gong

et al. 2018

American J Rep Immunol

View full text Add to dashboard Cite

Problem Premature birth complicates 10%–12% of deliveries. Infection and inflammation are the most common etiologies and are associated with increased offspring morbidity and mortality. We hypothesize that lipopolysaccharide (LPS)-induced maternal inflammation causes direct placenta injury and subsequent injury to the fetal intestine. Method of study Pregnant C57Bl6 mice were injected intraperitoneally on day 15.5 with 100 μg/kg LPS or saline. Maternal serum, amniotic fluid, placental samples, and ileal samples of offspring were obtained assessed for inflammation and/or injury. Maternal placental ultrasounds were performed. Placental DNA was isolated for microbiome analysis. Results Maternal injection with LPS caused elevated IL- 1β, IL-10, IL-6, KC-GRO, and TNF. Placental tissue showed increased IL-1β, IL-6, and KC-GRO and decreased IL-10, but no changes were observed in amniotic fluid. Placental histology demonstrated LPS-induced increases in mineralization and necrosis, but no difference in placental blood flow. Most placentas had no detectable microbiome. Exposure to maternal LPS induced significant injury to the ilea of the offspring. Conclusion Lipopolysaccharide causes a maternal inflammatory response that is mirrored in the placenta. Placental histology demonstrates structural changes; however, placental blood flow is preserved. LPS also induces an indirect intestinal injury in the offspring that lasts beyond the neonatal period.

show abstract

Section: | Discussionmentioning

confidence: 99%

Lipopolysaccharide‐induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Fricke

Elgin

Gong

et al. 2018

American J Rep Immunol

View full text Add to dashboard Cite

show abstract

“…The other protein markers did not show any differences between the studied groups. This may suggest that expression profile in the cord blood does not fully reflect the profile observed in-situ [15].…”

Section: Comparison Of Gene Expression In the Cord Blood Between Subgmentioning

confidence: 91%

“…A Spanish group conducted a prospective cohort study comparing preterm (27-36 GA) or term (> 37 wks) deliveries after a threatened preterm labour with term deliveries without suspected preterm labour [15]. They used placental samples for mRNA analysis and cord blood for selected protein inflammatory markers.…”

Section: Comparison Of Gene Expression In the Cord Blood Between Subgmentioning

confidence: 99%

Comparison of whole genome expression profile between preterm and full-term newborns

et al. 2017

View full text Add to dashboard Cite

Objectives: Evaluate the time dependent expression of genes in preterm neonates and verify the influence of ontogenic maturation and the environmental factors on the gene expression after birth. Material and methods:The study was carried out on 20 full-term newborns and 62 preterm newborns (mean birth weight = 1002 [g] (SD: 247), mean gestational age = 27.2 weeks (SD: 1.9)). Blood samples were drawn from all the study participants at birth and at the 36th week postmenstrual age from the preterm group to assess whole genome expression in umbilical cord blood and in peripheral blood leukocytes, respectively. (SurePrint G3 Human Gene Expression v3, 8x60K Microarrays (Agilent)).Results: A substantial number of genes was found to be expressed differentially at the time of birth and at 36 PMA in comparison to the term babies with more genes being down-regulated than up-regulated. However, the fold change in the majority of cases was < 2.0. Extremely preterm and very preterm infants were characterized by significantly down-regulated cytokine and chemokine related pathways. The number of down-regulated genes decreased and number of up-regulated genes increased at 36 PMA vs. cord blood. There were no specific gene expression pathway profiles found within the groups of different gestational ages. Conclusions:Preterm delivery is associated with a different gene expression profile in comparison to term delivery. The gene expression profile changes with the maturity of a newborn measured by the gestational age.

show abstract

“…After 24h, excess RNAlater was removed, and the samples were stored at -80°C. Tissue was homogenized, RNA was extracted, treated with DNase I, repurified and resuspended as previously described [26]. Concentrations were measured using Nanodrop, 100 ng of RNA was used in downstream PCR analysis.…”

Section: Methodsmentioning

confidence: 99%

High viral SARS-CoV-2 load in placenta of patients with hypertensive disorders after COVID-19 during pregnancy

Fabre¹,

Calvo

Ruiz

et al. 2021

Preprint

View full text Add to dashboard Cite

Introduction: Studies described an increased frequency of hypertensive disorders of pregnancy after a COVID-19 episode. There is limited evidence about SARS-CoV-2 viral load in placenta. This study aimed to investigate the relationship between SARS-CoV-2 viral load in placenta and clinical development of HDP after COVID-19 throughout different periods of gestation. Methods: This was a case-control study in women with and without gestational hypertensive disorders (HDP) after SARS-CoV-2 infection diagnosed by RT-PCR during pregnancy. Patients were matched by gestational age at the moment of COVID-19 diagnosis. We performed an analysis of SARS-CoV-2 RNA levels in placenta. Results: A total of 28 women were enrolled. Sixteen patients were diagnosed with COVID-19 during the third trimester and the remaining twelve patients in the others trimesters. Ten placentas (35.7%) were positive for SARS-CoV-2, nine of them (90%) belonged to the HDP group versus one (10%) in control group (p=0.009). Those cases with the highest loads of viral RNA developed severe-preeclampsia. Conclusion: The presence of SARS-CoV-2 was more frequent in placentas of patients with HDP after COVID-19. There seems to be a relationship between high viral load in the placenta and the development of hypertensive disorders. We found SARS-CoV-2 viral load in placenta after birth in mothers infected at the first half of pregnancy, but with negative nasopharyngeal RT-PCR at delivery. Our data suggest that SARS-CoV-2 infection during pregnancy could trigger gestational hypertensive disorders through placenta-related mechanisms.

show abstract

Altered gene expression in human placenta after suspected preterm labour

Cited by 19 publications

References 33 publications

Lipopolysaccharide‐induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Lipopolysaccharide‐induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Comparison of whole genome expression profile between preterm and full-term newborns

High viral SARS-CoV-2 load in placenta of patients with hypertensive disorders after COVID-19 during pregnancy

Contact Info

Product

Resources

About