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Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

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A decrease in DKK1, a WNT inhibitor, contributes to placental lipid accumulation in an obesity-prone rat model.

Rita S Strakovsky1, Yuan-Xiang Pan

  • 1Department of Food Science and Human Nutrition, University of Illinois, Urbana-Champaign, Urbana, Illinois 61801, USA.

Biology of Reproduction
|December 3, 2011
PubMed
Summary

Maternal obesity in rats leads to placental lipid accumulation and altered gene expression, impacting fetal development. Dickkopf homolog 1 (DKK1) plays a key role in regulating placental lipid metabolism via the WNT signaling pathway.

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Area of Science:

  • Reproductive biology
  • Developmental biology
  • Metabolic disorders

Background:

  • The placenta is crucial for nutrient transport and maternal-fetal health.
  • Maternal obesity can negatively impact placental function and offspring outcomes.
  • Understanding placental lipid metabolism is vital for addressing pregnancy complications.

Purpose of the Study:

  • To investigate the effects of maternal obesity on placental lipid accumulation and metabolism.
  • To explore the role of Dickkopf homolog 1 (DKK1) and WNT signaling in placental lipid regulation.
  • To identify key genes involved in placental lipid transport and synthesis.

Main Methods:

  • Comparison of obesity-prone (OP) and obesity-resistant (OR) rat strains during gestation.
  • Analysis of placental tissue for lipid accumulation, gene expression (mRNA), and protein localization.
  • In vitro studies using JEG3 trophoblast cells to assess DKK1's effect on lipid metabolism.

Main Results:

  • Obese dams exhibited elevated plasma and placental nonesterified fatty acids and triglycerides.
  • Placentas from OP dams showed reduced DKK1 mRNA, increased beta-catenin, and altered expression of lipid metabolism genes.
  • Significant lipid accumulation and reduced decidual/junctional zone thickness were observed in OP placentas.
  • DKK1 overexpression in JEG3 cells reduced lipid accumulation and key lipid metabolism gene expression.

Conclusions:

  • Maternal obesity induces placental lipid dysregulation, potentially mediated by DKK1.
  • DKK1 influences placental lipid transport and synthesis through the WNT signaling pathway.
  • These findings highlight DKK1 as a potential target for managing obesity-related placental complications.