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TNF-alpha expression in embryos exposed to a teratogen
I Ivnitsky1, A Torchinsky, M Gorivodsky
1Department of Embryology and Teratology, Sackler School of Medicine, Tel Aviv University, Israel.
American Journal of Reproductive Immunology (New York, N.Y. : 1989)
|January 23, 1999
Summary
Embryonic tumor necrosis factor-alpha (TNF-alpha) may drive craniofacial anomalies after cyclophosphamide exposure. Maternal immunostimulation reduced anomalies by decreasing embryonic TNF-alpha expression.
Area of Science:
- Developmental biology
- Immunology
- Toxicology
Background:
- The role of embryonic tumor necrosis factor-alpha (TNF-alpha) in development is unclear.
- Cyclophosphamide (CP) is a known teratogen causing developmental abnormalities.
Purpose of the Study:
- To investigate the involvement of TNF-alpha in CP-induced dysmorphogenesis.
- To assess the impact of maternal immunostimulation on embryonic TNF-alpha expression and teratogenic outcomes.
Main Methods:
- ICR mice were treated with CP on day 12 of pregnancy.
- Maternal immunostimulation was administered before mating.
- Embryos were analyzed for TNF-alpha and TNF-alpha receptor (TNFRI) mRNA and protein expression using in situ hybridization and immunostaining.
Main Results:
- CP-induced severe brain and craniofacial anomalies were observed.
- Elevated TNF-alpha and TNFR1 expression in embryonic brain and head preceded anomalies.
- Immunostimulation reduced anomaly severity and decreased TNF-alpha expression.
Conclusions:
- Embryonic TNF-alpha may promote CP-induced brain and craniofacial malformations.
- Reduced embryonic TNF-alpha expression is a potential mechanism for increased tolerance to teratogens.