To be, or not to be, that is the question. Apoptosis in human trophoblast

Placenta. 2000 Jan;21(1):1-13. doi: 10.1053/plac.1999.0450.

Abstract

Apoptosis, the morphology of cell suicide, may result from programmed cell death or may be a response to exogenous stimuli. Apoptosis can be induced in cultured trophoblast and can be identified in the trophoblast of placental villi. The trophoblast regulates maternal-fetal gas, nutrient and waste product exchange; therefore, the presence of apoptosis in this key cellular interface highlights the importance of understanding what controls apoptosis in the placenta. In this review, we describe the signal transduction pathways that trigger apoptosis in other systems, identify key genetic controls for the process and outline the final common pathway which effects execution in cells committed to suicide. Multiplicity, redundancy and cross talk among pathways characterize the surface membrane signals and exogenous stimuli that trigger apoptosis in other cells. As each step in the apoptotic process is discussed, we describe what is known about the step in human placental villi. Recent studies suggest that a further understanding of receptor-mediated signalling pathways, the Bcl-2 regulators and the caspases and substrates involved in placental apoptosis will surely provide insights into both normal placental development and the placental dysfunction associated with some abnormal pregnancies.

Publication types

  • Review

MeSH terms

  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Caspases / physiology
  • Female
  • Humans
  • Models, Biological
  • Pregnancy
  • Pregnancy Complications / pathology
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Signal Transduction
  • Trophoblasts / cytology*
  • Trophoblasts / physiology

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Caspases