Premium
ORIGINAL ARTICLE: Effect of Maternal Immunopotentiation on Apoptosis‐Associated Molecules Expression in Teratogen‐Treated Embryos
Author(s) -
Savion Shoshana,
Aroch Ilan,
Mammon Keren,
Orenstein Hasida,
Fein Amos,
Torchinsky Arkady,
Toder Vladimir
Publication year - 2009
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2009.00757.x
Subject(s) - tunel assay , flow cytometry , apoptosis , terminal deoxynucleotidyl transferase , andrology , embryo , splenocyte , teratology , embryonic stem cell , deoxyuridine , cell growth , immune system , chemistry , biology , immunology , microbiology and biotechnology , pregnancy , medicine , fetus , biochemistry , dna , genetics , gene
Problem Potentiation of the maternal immune system was shown by us to affect the embryonic response to teratogenic insults. In order to understand better the mechanisms underlying that phenomenon, we explored the effect of maternal immunopotentiation by rat splenocytes on the early stages of the embryonic response to cyclophosphamide (CP). Method of study Immunopotentiated CP‐treated embryos were analysed for cell cycle changes by flow cytometry, while cell proliferation and apoptosis were assessed by 5′‐bromo‐2′‐deoxyuridine (BrdU) incorporation and terminal deoxynucleotidyl transferase (TdT)‐mediated dUTP‐biotin nick‐end labeling (TUNEL) respectively. The expression of the p65 subunit of NF‐κB, IκBα, Bax, bcl‐2 and p53 was assessed by flow cytometry. Results Exposure to CP resulted in significant growth retardation and in the appearance of cellular damage, a reduction in cell proliferation and the appearance of apoptotic cells, which were all found to be delayed in immunopotentiated embryos. In parallel, CP‐treated embryos demonstrated a reduction in the percentage of p65‐ or IκBα‐positive cells, while the percentage of bcl‐2‐ or p53‐positive cells increased initially and decreased later. Those changes were normalized by maternal immunopotentiation when tested at 24 hrs after exposure to the teratogen. Conclusion Our data implicate maternal immunopotentiation to protect the embryo against teratogenic insults, possibly through its effect on the expression of p65, bcl‐2 or p53.