Vessel remodelling, pregnancy hormones and extravillous trophoblast function

Chen, Jessie; Sheehan, Penelope M.; Brennecke, Shaun P.; Keogh, Rosemary

doi:10.1016/j.mce.2011.10.014

Cited by 99 publications

(55 citation statements)

References 90 publications

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“…That transcription was altered went along with our RNA profiling results that showed the differential expression of numerous genes and noneprotein-coding RNAs (Supplementary Figures 3e5). The results of this analysis also bolstered the evidence that vascular endothelial growth factor, 30,31 progesterone actions, 32 and disordered protein serine threonine kinase signaling (eg, downstream of vascular endothelial growth factor 33 ) are involved in sPE pathogenesis as related to STBs.…”

Section: Global Transcriptional Profiling Of Trophoblast Subtypes (Spsupporting

confidence: 52%

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Gormley

Ona

Kapidzic

et al. 2017

American Journal of Obstetrics and Gynecology

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BACKGROUND:The maternal signs of preeclampsia, which include the new onset of high blood pressure, can occur because of faulty placentation. We theorized that transcriptomic analyses of trophoblast subpopulations in situ would lend new insights into the role of these cells in preeclampsia pathogenesis. OBJECTIVE: Our goal was to enrich syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts from the placentas of severe preeclampsia cases. Total RNA was subjected to global transcriptional profiling to identify RNAs that were misexpressed compared with controls. STUDY DESIGN: This was a cross-sectional analysis of placentas from women who had been diagnosed with severe preeclampsia. Gestational age-matched controls were placentas from women who had a preterm birth with no signs of infection. Laser microdissection enabled enrichment of syncytiotrophoblasts, invasive cytotrophoblasts, or endovascular cytotrophoblasts. After RNA isolation, a microarray approach was used for global transcriptional profiling. Immunolocalization identified changes in messenger RNA expression that carried over to the protein level. Differential expression of noneprotein-coding RNAs was confirmed by in situ hybridization. A 2-way analysis of variance of non-coding RNA expression identified particular classes that distinguished trophoblasts in cases vs controls. Cajal body foci were visualized by coilin immunolocalization. RESULTS: Comparison of the trophoblast subtype data within each group (severe preeclampsia or noninfected preterm birth) identified many highly differentially expressed genes. They included molecules that are known to be expressed by each subpopulation, which is evidence that the method worked. Genes that were expressed differentially between the 2 groups, in a cell-typeespecific manner, encoded a combination of molecules that previous studies associated with severe preeclampsia and those that were not known to be dysregulated in this pregnancy

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Section: Global Transcriptional Profiling Of Trophoblast Subtypes (Spsupporting

confidence: 52%

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Gormley

Ona

Kapidzic

et al. 2017

American Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

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“…Trophoblasts, as the main component of chorionic villi, play a leading role in the process. Therefore, the behaviors of trophoblasts, such as the proliferation, viability and invasion are vitally important (Chen et al 2012). Even though a lot of researches have been done to study the biological changes of trophoblasts in embryo implantation, the mechanism has not been fully illustrated yet.…”

Section: Discussionmentioning

confidence: 99%

“…Both E and hCG are synthesized by trophoblasts, and hCG can maintain the production of P by the corpus luteum (Chen et al 2012). P and hCG are classically known for their stimulatory roles in trophoblasts invasion and functional differentiation (Halasz & Szekeres-Bartho 2013).…”

Section: Discussionmentioning

confidence: 99%

“…The receptor of estrogen ERa was found in differentiating cytotrophoblast cells of term placenta (Bukovsky et al 2003). Nevertheless, it was proposed that E might not have significant impact on trophoblasts based on the fact that E deficiency usually did not result in fetal abnormalities (Chen et al 2012). Chen et al (2011) found that hCG stimulated the migration of cells but did not affect cell number, high dose of P inhibited the migration of trophoblast cell line HTR8/SVneo as well as the number of cells, but E had no effect.…”

Section: Discussionmentioning

confidence: 99%

“…When fetal-derived villi contact with maternal decidua, a subpopulation of trophoblasts located at the tips of anchoring villi undergo proliferation and differentiation, and develop into invasive extravillous trophoblasts (EVTs). Finally, EVTs infiltrate into decidual spiral arteries to remodel the vessel walls (Chen et al 2012). The entire process is precisely regulated by modulators at the maternal-fetal interface; for example, decidual immune cells (DICs), DSCs, female steroid hormones and cytokines (Paiva et al 2011, Oreshkova et al 2012.…”

Section: Introductionmentioning

confidence: 99%

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Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Meng

Shang

et al. 2015

Reproduction

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Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation. Reproduction (2015) 150 417-427

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Uterine Vasculature Remodeling in Human Pregnancy Involves Functional Macrochimerism by Endothelial Colony Forming Cells of Fetal Origin

et al. 2013

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The potency of adult-derived circulating progenitor endothelial colony forming cells (ECFCs) is drastically surpassed by their fetal counterparts. Human pregnancy is associated with robust intensification of blood flow and vascular expansion in the uterus, crucial for placental perfusion and fetal supply. Here, we investigate whether fetal ECFCs transmigrate to maternal bloodstream and home to locations of maternal vasculogenesis, primarily the pregnant uterus. In the first instance, endothelial-like cells, originating from mouse fetuses expressing paternal eGFP, were identified within uterine endothelia. Subsequently, LacZ or enhanced green fluorescent protein (eGFP)-labeled human fetal ECFCs, transplanted into immunodeficient (NOD/SCID) fetuses on D15.5 pregnancy, showed similar integration into the mouse uterus by term. Mature endothelial controls (human umbilical vein endothelial cells), similarly introduced, were unequivocally absent. In humans, SRY was detected in 6 of 12 myometrial microvessels obtained from women delivering male babies. The copy number was calculated at 175 [IQR 149–471] fetal cells per millimeter square endothelium, constituting 12.5% of maternal vessel lumina. Cross-sections of similar human vessels, hybridized for Y-chromosome, positively identified endothelial-associated fetal cells. It appears that through ECFC donation, fetuses assist maternal uterine vascular expansion in pregnancy, potentiating placental perfusion and consequently their own fetal supply. In addition to fetal growth, this cellular mechanism holds implications for materno-fetal immune interactions and long-term maternal vascular health.

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Vessel remodelling, pregnancy hormones and extravillous trophoblast function

Cited by 99 publications

References 90 publications

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Preeclampsia: novel insights from global RNA profiling of trophoblast subpopulations

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Uterine Vasculature Remodeling in Human Pregnancy Involves Functional Macrochimerism by Endothelial Colony Forming Cells of Fetal Origin

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