Immunohistochemical expression of p57 in placental vascular proliferative disorders of preterm and term placentas

Fetal Pediatr Pathol. 2009;28(1):9-23. doi: 10.1080/15513810802545350.

Abstract

P57 protein is implicated in some human imprinting disorders such as hydatiform mole and Beckwith-Wiedemann syndrome (BWS), both characterized by mesenchymal and vascular placental abnormalities. We investigated p57 immunohistochemical expression in placental vascular proliferative disorders of preterm and term placentas, including chorangiosis (n = 5), chorangiomatosis (n = 2), chorangiomas (n = 7), umbilical cord angioma (n = 1), and placental mesenchymal dysplasia (PMD) (n = 7). P57 was expressed in decidua, cytotrophoblast, intermediate trophoblast and stromal cells of normal terminal, intermediate and stem villi, umbilical cord, chorangiosis, chorangiomatosis, and chorangiomas. In contrast, there was a loss of p57 expression in stromal cells of dysplastic stem villi in all cases of PMD regardless of whether associated with BWS or not. P57 seems to be involved in the pathogenesis of a subset of placental vascular proliferative disorders in preterm and term placentas, such as PMD. The loss of p57 expression in PMD could be of diagnostic value in helping to distinguish this rare placental lesion from its mimickers.

MeSH terms

  • Adult
  • Biomarkers / analysis
  • Cyclin-Dependent Kinase Inhibitor p57 / biosynthesis*
  • Female
  • Humans
  • Immunohistochemistry
  • Placenta / metabolism
  • Placenta / pathology
  • Placenta Diseases / diagnosis*
  • Placenta Diseases / metabolism*
  • Placenta Diseases / pathology
  • Pregnancy
  • Premature Birth
  • Vascular Diseases / diagnosis*
  • Vascular Diseases / metabolism*
  • Vascular Diseases / pathology

Substances

  • Biomarkers
  • CDKN1C protein, human
  • Cyclin-Dependent Kinase Inhibitor p57