Mechanism of programmed cell death in the blastocyst.

Abstract

The malignant growth potential of embryonal carcinoma cells may be controlled by environmental factors. For example, embryonal carcinoma cells placed into normal blastocysts may not exhibit the continued growth expected of malignant cells but rather may lose all aspects of the malignant phenotype and become apparently normal embryonic cells. Loss of the malignant phenotype of embryonal carcinoma cells occurs early in these I jected blastocysts and has been used as the basis of assays to study the mechanisms of regulation of embryonal carcinoma by the blastocyst. In this regard, P19, an embryonal carcinoma that makes midgestation chimeras, was regulated by blastocele fluid plus contact with trophectoderm but not by blastocele fluid plus contact with inner cell mass (ICM). In contrast, ECa 247, which makes trophectoderm, was regulated by exposure to blastocele fluid plus contact with trophectoderm or ICM. During the course of these experiments, dead embryonal carcinoma and ICM cells were observed, and blastocele fluid was then shown to kill ECa 247 and normal ICM cells of early blastocysts with trophectodermal potential. P19 cells and ICM cells with potential to make the embryo were not killed by blastocele fluid. Programmed cell death occurs in the ICM of the blastocyst during the transition from early (when ICM has the potential to make trophectoderm) to late (when the ICM lacks the potential to make trophectoderm). It is postulated that this programmed cell death is designed to eliminate redundant 1CM cells with trophectodermal potential, and its mechanism of action is mediated by epigenetic factors in blastocele fluid.zP T E _G

Cell death in the avian blastoderm: resistance to stress-induced apoptosis and expression of anti-apoptotic genes

“…In the mammalian blastocyst, some inner cell mass cells with the potential to form trophoectoderm die by apoptosis, and this may represent a mechanism for eliminating redundant cells (Pierce et al, 1989). It would seem hazardous for early embryo cells to have a suicide capacity, but this may be counteracted by the expression of one or more anti-apoptotic regulatory genes and cytoprotective systems.…”

Tiam1 is involved in the regulation of bufalin-induced apoptosis in human leukemia cells

“…Apoptosis is thought to play a key role in embryogenesis (Pierce et al, 1989), carcinogenesis (Vaux et al, 1988), and the killing of virally infected cells (Laurent-Crawford et al, 1991). Although apoptosis is initiated by many physiological and pathological stimuli, all apoptotic cells undergo a similar sequence of morphological and biochemical events (Martin et al, 1994), which include condensation of the chromatin in the nucleus; fragmentation of DNA into fragments with lengths that are multiples of approximately 180 bp, as a result of speci®c cleavage between nucleosomes by an endogenous endonuclease; and a relatively high degree of preservation of the plasma membrane and cytoplasmic organelles.…”

Glucose utilization and the PI3-K pathway: mechanisms for cell survival in preimplantation embryos

“…In mammalian development, apoptosis normally occurs at the blastocyst stage and arises in both the ICM and TE (Mohr & Trounson 1982, Handyside & Hunter 1986, Brison & Schultz 1997, Jurisicova et al 1998. During this stage of development, one purpose of programmed cell death may be to eliminate cells with TE potential from the ICM (Pierce et al 1989). There are many insults that induce apoptosis in the preimplantation embryo, one of which is glucose deprivation.…”