Double-label immunohistochemistry to assess labyrinth structure of the mouse placenta with stereology

Clercq, Katrien De; López-Tello, Jorge; Vriens, Joris; Sferruzzi‐Perri, Amanda N.

doi:10.1016/j.placenta.2020.03.014

Cited by 23 publications

(28 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Placental stereology for Igf2 HCKO model was performed as described ( De Clercq et al., 2020 ). Briefly, placental samples were embedded in paraffin as described above, sectioned, and then double-labelled for lectin and cytokeratin, which allows the identification of Lz constituents.…”

Section: Methodsmentioning

confidence: 99%

The imprinted Igf2-Igf2r axis is critical for matching placental microvasculature expansion to fetal growth

et al. 2022

Self Cite

View full text Add to dashboard Cite

Summary In all eutherian mammals, growth of the fetus is dependent upon a functional placenta, but whether and how the latter adapts to putative fetal signals is currently unknown. Here, we demonstrate, through fetal, endothelial, hematopoietic, and trophoblast-specific genetic manipulations in the mouse, that endothelial and fetus-derived IGF2 is required for the continuous expansion of the feto-placental microvasculature in late pregnancy. The angiocrine effects of IGF2 on placental microvasculature expansion are mediated, in part, through IGF2R and angiopoietin-Tie2/TEK signaling. Additionally, IGF2 exerts IGF2R-ERK1/2-dependent pro-proliferative and angiogenic effects on primary feto-placental endothelial cells ex vivo . Endothelial and fetus-derived IGF2 also plays an important role in trophoblast morphogenesis, acting through Gcm1 and Synb . Thus, our study reveals a direct role for the imprinted Igf2-Igf2r axis on matching placental development to fetal growth and establishes the principle that hormone-like signals from the fetus play important roles in controlling placental microvasculature and trophoblast morphogenesis.

show abstract

Section: Methodsmentioning

confidence: 99%

The imprinted Igf2-Igf2r axis is critical for matching placental microvasculature expansion to fetal growth

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

“…Morphology of the Lz was assessed by double-labelling placental sections with cytokeratin and lectin antibodies to identify trophoblast and fetal capillaries, respectively. Details about the staining protocol have been described in detail elsewhere [28]. Stained sections were then scanned using a NanoZoomer 2.0-RS Digital Pathology System (NDP Scan Hamamatsu, Japan) and stereological analysis of the Lz was performed as described previously [28].…”

Section: Placental Lz Structural Analysismentioning

confidence: 99%

“…Details about the staining protocol have been described in detail elsewhere [28]. Stained sections were then scanned using a NanoZoomer 2.0-RS Digital Pathology System (NDP Scan Hamamatsu, Japan) and stereological analysis of the Lz was performed as described previously [28].…”

Section: Placental Lz Structural Analysismentioning

confidence: 99%

Placental structure, function and mitochondrial phenotype relate to fetal size and sex in mice

Salazar‐Petres

Carvalho

López-Tello

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

Fetal growth depends on placental function, which requires energy supplied by mitochondria. Here we investigated whether mitochondrial function in the placenta relates to growth of the lightest and heaviest fetuses of each sex within the litter of mice. Placentas from the lightest and heaviest fetuses were taken to evaluate placenta morphology (stereology), mitochondrial energetics (high-resolution respirometry), and mitochondrial regulators, nutrient transporters, hormone handling and signalling pathways (qPCR and western blotting). We found that mitochondrial complex I and II oxygen consumption rate was greater for placentas supporting the lightest female fetuses, although placental complex I abundance of the lightest females and complexes III and V of the lightest males were decreased compared to their heaviest counterparts. Expression of mitochondrial biogenesis (Nrf1) and fission (Drp1 and Fis1) genes was lower in the placenta from the lightest females, whilst biogenesis-related gene Tfam was greater in the placenta of the lightest male fetuses. Additionally, placental morphology and steroidogenic gene (Cyp17a1 and Cyp11a1) expression were aberrant for the lightest females, but glucose transporter (Glut1) expression lower in only the lightest males versus their heaviest counterparts. Differences in intra-litter placental phenotype were related to sex-dependent changes in the expression of hormone responsive (androgen receptor) and metabolic signalling pathways (AMPK, AKT, PPARγ). Thus, in normal mouse pregnancy, placental structure, function and mitochondrial phenotype are differentially responsive to growth of the female and the male fetus. This study may inform the design of sex-specific therapies for placental insufficiency and fetal growth abnormalities with life-long benefits for the offspring.

show abstract

“…For analysis of labyrinth components, sections were stained with lectin for identification of fetal endothelial vessels and with cytokeratin for trophoblasts. Further details of the double-labelling immunohistochemistry and the analysis performed can be found elsewhere (36). For the analysis of placental glycogen, sections were stained with Periodic acid-Schiff (Sigma-Aldrich) previous incubation with 0.5% periodic acid (Thermo Fisher Scientific).…”

Section: Placental Histologymentioning

confidence: 99%

Maternal gut microbiota Bifidobacterium promotes placental morphogenesis, nutrient transport and fetal growth in mice

López-Tello

Schofield

Kiu

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

The gut microbiota plays a central role in regulating host metabolism. However, while substantial progress has been made in discerning how the microbiota influences host functions post birth and beyond, little has been carried out into understanding how key members of the maternal gut microbiota can influence feto-placental growth. Here, using germ-free and specific-pathogen-free mice, we demonstrate that the bacterium Bifidobacterium breve UCC2003 modulates maternal body adaptations, placental vasculature growth and nutrient transporter capacity, with implications for fetal metabolism and growth. The effects of B. breve UCC2003 on feto-placental growth are mediated, in part, by changes in the maternal and placental metabolome (i.e. acetate and carnitine). Analysis of placental vascular bed confirmed that Bifidobacterium improves fetal capillary elongation via changes in Igf2P0, Dlk1 and Mapk14 expression. Additionally, B. breve UCC2003, acting through Slc2a1 and Fatp3-4 transporters, was shown to restore fetal glycaemia and improve fetal growth in association with changes in the fetal hepatic transcriptome. This study provides knowledge towards a novel and safe therapeutic strategy for treating pregnancy disorders via modulation of the maternal gut microbiota.

show abstract

Double-label immunohistochemistry to assess labyrinth structure of the mouse placenta with stereology

Cited by 23 publications

References 17 publications

The imprinted Igf2-Igf2r axis is critical for matching placental microvasculature expansion to fetal growth

The imprinted Igf2-Igf2r axis is critical for matching placental microvasculature expansion to fetal growth

Placental structure, function and mitochondrial phenotype relate to fetal size and sex in mice

Maternal gut microbiota Bifidobacterium promotes placental morphogenesis, nutrient transport and fetal growth in mice

Contact Info

Product

Resources

About