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D2-40/podoplanin expression in the human placenta.

Y Wang1, J Sun, Y Gu

  • 1Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center, Shreveport, LA, USA. ywang1@lsuhsc.edu

Placenta
|November 25, 2010
PubMed
Summary
This summary is machine-generated.

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The human placenta expresses D2-40/podoplanin, a lymphatic marker, forming a network in the villous stroma. Preeclampsia reduces D2-40/podoplanin and increases VEGFR-3, potentially impacting placental function.

Area of Science:

  • Obstetrics and Gynecology
  • Vascular Biology
  • Cell Biology

Background:

  • Lymphatic markers are expressed in placental tissue.
  • D2-40/podoplanin is a lymphatic endothelial marker.
  • Its role and expression patterns in the placenta are not fully understood.

Purpose of the Study:

  • To investigate the expression of D2-40/podoplanin in the human placenta.
  • To determine how D2-40/podoplanin expression changes during pregnancy development and in preeclampsia.
  • To examine the expression of VEGFR-3 in relation to D2-40/podoplanin.

Main Methods:

  • Western blot analysis of placental tissue from normotensive and preeclamptic pregnancies.
  • Immunohistochemical examination of D2-40/podoplanin and VEGFR-3.

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  • Comparison of protein expression levels between groups.

    • Main Results:

    • D2-40/podoplanin was strongly expressed in the placental villous stroma in a network pattern throughout gestation.
    • CD31 was localized to fetal vessel endothelium, while VEGFR-3 was found in fetal vessel endothelium and trophoblasts.
    • D2-40/podoplanin expression was significantly decreased, and VEGFR-3 significantly increased in preeclamptic placentas compared to normotensive controls.

    Conclusions:

    • The localization of D2-40/podoplanin suggests a potential lymphatic-like conductive network within the human placenta.
    • Reduced D2-40/podoplanin in preeclampsia may contribute to altered fluid homeostasis and impaired angiogenesis.
    • Placental D2-40/podoplanin may play a role in fetal vessel angiogenesis during placental development.