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Updated: Dec 5, 2025

Isolation of Primary Mouse Trophoblast Cells and Trophoblast Invasion Assay
Published on: January 8, 2012
Regulation of trophoblast cell invasion by Pyruvate Kinase isozyme M2 (PKM2)
Kary Y F Tsai1, Benton Tullis1, Juan Mejia1
1Lung and Placenta Research Laboratory, Brigham Young University, Department of Physiology and Developmental Biology, Provo, UT, USA.
Abstract:
The Pyruvate kinase isozymes M2 (PKM2) protein is a metabolic enzyme that regulates the final step of glycolysis. This enzyme is present in highly proliferating cells and is expressed in the placenta. We recently demonstrated upregulated placental PKM2 during human intrauterine growth restriction (IUGR). Our current objective was to determine PKM2 regulation of trophoblast invasion, trophoblast PKM2 localization as well as mTOR protein expression, and to determine effects of activation of PKM2 during IUGR. Human placental tissues were obtained and analyzed by immunohistochemistry and western blot. Trophoblast cells were cultured in normoxic and hypoxic conditions and real time cell invasion and PKM2 protein were determined during activation (Fructose-6-bisphosphate; FBP6) or inhibition (Shikonin) of PKM2. In vivo studies determined the effects of PKM2 activation on placental and fetal weights. IUGR samples had elevated levels of p-PKM2. Different trophoblast PKM2 localization and expression was observed during normoxia and hypoxia. Decreased trophoblast invasion and PKM2 expression was observed during mTOR inhibition. Protection from decreased placental and fetal weights was observed by PKM2 activation. We conclude that PKM2 regulates trophoblast cell invasion depending on its subcellular location. Our results suggest that PKM2 regulation in trophoblast cells is more directly affected during hypoxia and its expression is regulated by mTOR activity. Additionally, we conclude that activation of PKM2 could reverse and/or rescue the deceased placental and fetal weights observed during IUGR. These results suggest that PKM2 could be a mediator of trophoblast cell invasion and its abundance influences the development of complicated pregnancies like IUGR.
Insights
Pyruvate kinase M2 (PKM2) regulates trophoblast invasion, impacting placental development in intrauterine growth restriction (IUGR). Activating PKM2 may reverse IUGR-related weight loss, suggesting its therapeutic potential.
Area of Science:
- Cell Biology
- Metabolic Regulation
- Reproductive Medicine
Background:
- Pyruvate kinase isozymes M2 (PKM2) is a key glycolytic enzyme found in proliferating cells, including the placenta.
- Upregulated placental PKM2 has been observed in human intrauterine growth restriction (IUGR).
Purpose of the Study:
- To investigate PKM2's role in trophoblast invasion and localization.
- To examine PKM2's regulation by mTOR signaling.
- To assess the therapeutic potential of PKM2 activation in IUGR models.
Main Methods:
- Immunohistochemistry and Western blot analysis of human placental tissues.
- In vitro culture of trophoblast cells under normoxic and hypoxic conditions.
- Assessment of cell invasion, PKM2 expression, and mTOR activity.
- In vivo studies evaluating PKM2 activation effects on placental and fetal weights.
Main Results:
- Elevated phosphorylated PKM2 (p-PKM2) levels in IUGR samples.
- Differential trophoblast PKM2 localization and expression under varying oxygen conditions.
- mTOR inhibition decreased trophoblast invasion and PKM2 expression.
- PKM2 activation protected against reduced placental and fetal weights in vivo.
Conclusions:
- PKM2 regulates trophoblast invasion, influenced by its subcellular localization and cellular oxygen levels.
- mTOR signaling modulates trophoblast PKM2 expression and activity.
- PKM2 activation demonstrates potential to counteract IUGR-associated growth deficits, highlighting its role in complicated pregnancies.
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